Journal of Athletic Training
2002;37(1):99–104
q by the National Athletic Trainers’ Association, Inc
www.journalofathletictraining.org
National Athletic Trainers’ Association
Position Statement: Emergency Planning
in Athletics
J. C. Andersen*; Ronald W. Courson†; Douglas M. Kleiner‡;
Todd A. McLoda§
*Armstrong Atlantic State University, Savannah, GA; †University of Georgia, Athens, GA; ‡University of Florida,
Health Science Center/Jacksonville, Jacksonville, FL; §Illinois State University, Normal, IL
J. C. Andersen, PhD, ATC, PT, SCS, contributed to conception and design; acquisition and analysis and interpretation of the
data; and drafting, critical revision, and final approval of the article. Ronald W. Courson, ATC, PT, NREMT-I, CSCS, Douglas
M. Kleiner, PhD, ATC, CSCS, NREMT, FACSM, and Todd A. McLoda, PhD, ATC, contributed to acquisition and analysis and
interpretation of the data and drafting, critical revision, and final approval of the article.
Address correspondence to National Athletic Trainers’ Association, Communications Department, 2952 Stemmons Freeway,
Dallas, TX 75247.
Objectives: To educate athletic trainers and others about the
need for emergency planning, to provide guidelines in the development of emergency plans, and to advocate documentation
of emergency planning.
Background: Most injuries sustained during athletics or other physical activity are relatively minor. However, potentially
limb-threatening or life-threatening emergencies in athletics and
physical activity are unpredictable and occur without warning.
Proper management of these injuries is critical and should be
carried out by trained health services personnel to minimize risk
to the injured participant. The organization or institution and its
personnel can be placed at risk by the lack of an emergency
plan, which may be the foundation of a legal claim.
Recommendations: The National Athletic Trainers’ Association recommends that each organization or institution that
sponsors athletic activities or events develop and implement a
written emergency plan. Emergency plans should be developed
by organizational or institutional personnel in consultation with
the local emergency medical services. Components of the
emergency plan include identification of the personnel involved,
specification of the equipment needed to respond to the emergency, and establishment of a communication system to summon emergency care. Additional components of the emergency
plan are identification of the mode of emergency transport,
specification of the venue or activity location, and incorporation
of emergency service personnel into the development and implementation process. Emergency plans should be reviewed
and rehearsed annually, with written documentation of any
modifications. The plan should identify responsibility for documentation of actions taken during the emergency, evaluation of
the emergency response, institutional personnel training, and
equipment maintenance. Further, training of the involved personnel should include automatic external defibrillation, cardiopulmonary resuscitation, first aid, and prevention of disease
transmission.
Key Words: policies and procedures, athletics, planning, catastrophic
A
nel, and the formation and implementation of an emergency
plan. The emergency plan should be thought of as a blueprint
for handling emergencies. A sound emergency plan is easily
understood and establishes accountability for the management
of emergencies. Furthermore, failure to have an emergency
plan can be considered negligence.5
lthough most injuries that occur in athletics are relatively minor, limb-threatening or life-threatening injuries are unpredictable and can occur without warning.1 Because of the relatively low incidence rate of catastrophic injuries, athletic program personnel may develop a
false sense of security over time in the absence of such injuries.1–4 However, these injuries can occur during any physical
activity and at any level of participation. Of additional concern
is the heightened public awareness associated with the nature
and management of such injuries. Medicolegal interests can
lead to questions about the qualifications of the personnel involved, the preparedness of the organization for handling these
situations, and the actions taken by program personnel.5
Proper emergency management of limb- or life-threatening
injuries is critical and should be handled by trained medical
and allied health personnel.1–4 Preparation for response to
emergencies includes education and training, maintenance of
emergency equipment and supplies, appropriate use of person-
POSITION STATEMENT
Based on an extensive survey of the literature and expert
review, the following is the position of the National Athletic
Trainers’ Association (NATA):
1. Each institution or organization that sponsors athletic activities must have a written emergency plan. The emergency plan should be comprehensive and practical, yet
flexible enough to adapt to any emergency situation.
2. Emergency plans must be written documents and should
be distributed to certified athletic trainers, team and at-
Journal of Athletic Training
99
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
tending physicians, athletic training students, institutional
and organizational safety personnel, institutional and organizational administrators, and coaches. The emergency
plan should be developed in consultation with local emergency medical services personnel.
An emergency plan for athletics identifies the personnel
involved in carrying out the emergency plan and outlines
the qualifications of those executing the plan. Sports medicine professionals, officials, and coaches should be
trained in automatic external defibrillation, cardiopulmonary resuscitation, first aid, and prevention of disease
transmission.
The emergency plan should specify the equipment needed
to carry out the tasks required in the event of an emergency. In addition, the emergency plan should outline the
location of the emergency equipment. Further, the equipment available should be appropriate to the level of training of the personnel involved.
Establishment of a clear mechanism for communication to
appropriate emergency care service providers and identification of the mode of transportation for the injured participant are critical elements of an emergency plan.
The emergency plan should be specific to the activity venue. That is, each activity site should have a defined emergency plan that is derived from the overall institutional or
organizational policies on emergency planning.
Emergency plans should incorporate the emergency care
facilities to which the injured individual will be taken.
Emergency receiving facilities should be notified in advance of scheduled events and contests. Personnel from
the emergency receiving facilities should be included in
the development of the emergency plan for the institution
or organization.
The emergency plan specifies the necessary documentation supporting the implementation and evaluation of the
emergency plan. This documentation should identify responsibility for documenting actions taken during the
emergency, evaluation of the emergency response, and institutional personnel training.
The emergency plan should be reviewed and rehearsed
annually, although more frequent review and rehearsal
may be necessary. The results of these reviews and rehearsals should be documented and should indicate whether the emergency plan was modified, with further documentation reflecting how the plan was changed.
All personnel involved with the organization and sponsorship of athletic activities share a professional responsibility to provide for the emergency care of an injured
person, including the development and implementation of
an emergency plan.
All personnel involved with the organization and sponsorship of athletic activities share a legal duty to develop,
implement, and evaluate an emergency plan for all sponsored athletic activities.
The emergency plan should be reviewed by the administration and legal counsel of the sponsoring organization
or institution.
BACKGROUND FOR THIS POSITION STAND
Need for Emergency Plans
Emergencies, accidents, and natural disasters are rarely predictable; however, when they do occur, rapid, controlled re-
100
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• Number 1 • March 2002
sponse will likely make the difference between an effective
and an ineffective emergency response. Response can be hindered by the chaotic actions and increased emotions of those
who make attempts to help persons who are injured or in danger. One method of control for these unpredictable events is
an emergency plan that, if well designed and rehearsed, can
provide responders with an organized approach to their reaction. The development of the emergency plan takes care and
time to ensure that all necessary contingencies have been included. Lessons learned from major emergencies are also important to consider when developing or revising an emergency
plan.
Emergency plans are applicable to agencies of the government, such as law enforcement, fire and rescue, and federal
emergency management teams. Furthermore, the use of emergency plans is directly applicable to sport and fitness activities
due to the inherent possibility of ‘‘an untoward event’’ that
requires access to emergency medical services.6 Of course,
when developing an emergency plan for athletics, there is one
notable difference from those used by local, state, and federal
emergency management personnel. With few exceptions, typically only one athlete, fan, or sideline participant is at risk at
one time due to bleeding, internal injury, cardiac arrest, shock,
or traumatic head or spine injury. However, emergency planning in athletics should account for an untoward event involving a game official, fan, or sideline participant as well as the
participating athlete. Although triage in athletic emergency situations may be rare, this does not minimize the risks involved
and the need for carefully prepared emergency care plans. The
need for emergency plans in athletics can be divided into 2
major categories: professional and legal.
Professional Need. The first category for consideration in
determining the need for emergency plans in athletics is organizational and professional responsibility. Certain governing
bodies associated with athletic competition have stated that
institutions and organizations must provide for access to emergency medical services if an emergency should occur during
any aspect of athletic activity, including in-season and offseason activities.6 The National Collegiate Athletic Association (NCAA) has recommended that all member institutions
develop an emergency plan for their athletic programs.7 The
National Federation of State High School Associations has
recommended the same at the secondary school level.8 The
NCAA states, ‘‘Each scheduled practice or contest of an institution-sponsored intercollegiate athletics event, as well as
out-of-season practices and skills sessions, should include an
emergency plan.’’6 The 1999–2000 NCAA Sports Medicine
Handbook further outlines the key components of the emergency plan.6
Although the 1999–2000 NCAA Sports Medicine Handbook
is a useful guide, a recent survey of NCAA member institutions revealed that at least 10% of the institutions do not maintain any form of an emergency plan.7 In addition, more than
one third of the institutions do not maintain emergency plans
for the off-season strength and conditioning activities of the
sports.
Personnel coverage at NCAA institutions was also found to
be an issue. Nearly all schools provided personnel qualified to
administer emergency care for high-risk contact sports, but
fewer than two thirds of institutions provided adequate personnel to sports such as cross-country and track.9 In a memorandum dated March 25, 1999, and sent to key personnel at
all schools, the president of the NCAA reiterated the recommendations in the 1999–2000 NCAA Sports Medicine Handbook to maintain emergency plans for all sport activities, including skill instruction, conditioning, and the nontraditional
practice seasons.8
A need for emergency preparedness is further recognized
by several national organizations concerned with the delivery
of health care services to fitness and sport participants, including the NATA Education Council,10 NATA Board of Certification, Inc,11 American College of Sports Medicine, International Health Racquet and Sports Club Association,
American College of Cardiology, and Young Men’s Christian
Association.12 The NATA-approved athletic training educational competencies for athletic trainers include several references to emergency action plans.10 The knowledge of the key
components of an emergency plan, the ability to recognize and
appraise emergency plans, and the ability to develop emergency plans are all considered required tasks of the athletic
trainer.11 These responsibilities justify the need for the athletic
trainer to be involved in the development and application of
emergency plans as a partial fulfillment of his or her professional obligations.
In addition to the equipment and personnel involved in
emergency response, the emergency plan must include consideration for the sport activity and rules of competition, the
weather conditions, and the level of competition.13 The variation in these factors makes venue-specific planning necessary
because of the numerous contingencies that may occur. For
example, many youth sport activities include both new participants of various sizes who may not know the rules of the
activity and those who have participated for years. Also, outdoor sport activities include the possibility of lightning strikes,
excessive heat and humidity, and excessive cold, among other
environmental concerns that may not be factors during indoor
activities. Organizations in areas of the country in which snow
may accumulate must consider provisions for ensuring that
accessibility by emergency vehicles is not hampered. In addition, the availability of safety equipment that is necessary
for participation may be an issue for those in underserved
areas. The burden of considering all the possible contingencies
in light of the various situations must rest on the professionals,
who are best trained to recognize the need for emergency plans
and who can develop and implement the venue-specific plans.
Legal Need. Also of significance is the legal basis for the
development and application of an emergency plan. It is well
known that organizational medical personnel, including certified athletic trainers, have a legal duty as reasonable and prudent professionals to ensure high-quality care of the participants. Of further legal precedence is the accepted standard of
care by which allied health professionals are measured.14 This
standard of care provides necessary accountability for the actions of both the practitioners and the governing body that
oversees those practitioners. The emergency plan has been categorized as a written document that defines the standard of
care required during an emergency situation.15 Herbert16 emphasized that well-formulated, adequately written, and periodically rehearsed emergency response protocols are absolutely required by sports medicine programs. Herbert16 further
stated that the absence of an emergency plan frequently is the
basis for claim and suit based on negligence.
One key indicator for the need for an emergency action plan
is the concept of foreseeability. The organization administrators and the members of the sports medicine team must ques-
tion whether a particular emergency situation has a reasonable
possibility of occurring during the sport activity in question.14,15,17 For example, if it is reasonably possible that a
catastrophic event such as a head injury, spine injury, or other
severe trauma may occur during practice, conditioning, or
competition in a sport, a previously prepared emergency plan
must be in place. The medical and allied health care personnel
must constantly be on guard for potential injuries, and although the occurrence of limb-threatening or life-threatening
emergencies is not common, the potential exists. Therefore,
prepared emergency responders must have planned in advance
for the action to be taken in the event of such an emergency.
Several legal claims and suits have indicated or alluded to
the need for emergency plans. In Gathers v Loyola Marymount
University,18 the state court settlement included a statement
that care was delayed for the injured athlete, and the plaintiffs
further alleged that the defendants acted negligently and carelessly in not providing appropriate emergency response. These
observations strongly support the need to have clear emergency plans in place, rehearsed, and carried out. In several additional cases,19–21 the courts have stated that proper care was
delayed, and it can be reasoned that these delays could have
been avoided with the application of a well-prepared emergency plan.
Perhaps the most significant case bearing on the need for
emergency planning is Kleinknecht v Gettysburg College,
which came before the appellate court in 1993.5,17 In a portion
of the decision, the court stated that the college owed a duty
to the athletes who are recruited to be athletes at the institution.
Further, as a part of that duty, the college must provide
‘‘prompt and adequate emergency services while engaged in
the school-sponsored intercollegiate athletic activity for which
the athlete had been recruited.’’17 The same court further ruled
that reasonable measures must be ensured and in place to provide prompt treatment of emergency situations. One can conclude from these rulings that planning is critical to ensure
prompt and proper emergency medical care, further validating
the need for an emergency plan.5
Based on the review of the legal and professional literature,
there is no doubt regarding the need for organizations at all
levels that sponsor athletic activities to maintain an up-to-date,
thorough, and regularly rehearsed emergency plan. Furthermore, members of the sports medicine team have both legal
and professional obligations to perform this duty to protect the
interests of both the participating athletes and the organization
or institution. At best, failure to do so will inevitably result in
inefficient athlete care, whereas at worst, gross negligence and
potential life-threatening ramifications for the injured athlete
or organizational personnel are likely.
Components of Emergency Plans
Organizations that sponsor athletic activities have a duty
to develop an emergency plan that can be implemented immediately and to provide appropriate standards of health care
to all sports participants.5,14,15,17 Athletic injuries may occur
at any time and during any activity. The sports medicine team
must be prepared through the formulation of an emergency
plan, proper coverage of events, maintenance of appropriate
emergency equipment and supplies, use of appropriate emergency medical personnel, and continuing education in the
area of emergency medicine. Some potential emergencies
may be averted through careful preparticipation physical
Journal of Athletic Training
101
Sample Venue-Specific Emergency Protocol
University Sports Medicine Football Emergency Protocol
1. Call 911 or other emergency number consistent with organizational policies
2. Instruct emergency medical services (EMS) personnel to ‘‘report to
and meet
at
as we have an
injured student-athlete in need of emergency medical treatment.’’
University Football Practice Complex:
Street entrance (gate across street from
) cross street:
Street
University Stadium: Gate
entrance off
Road
3. Provide necessary information to EMS personnel:
● name, address, telephone number of caller
● number of victims; condition of victims
● first-aid treatment initiated
● specific directions as needed to locate scene
● other information as requested by dispatcher
4. Provide appropriate emergency care until arrival of EMS personnel: on arrival of EMS personnel, provide pertinent information (method of
injury, vital signs, treatment rendered, medical history) and assist with emergency care as needed
Note:
●
●
●
●
●
●
sports medicine staff member should accompany student-athlete to hospital
notify other sports medicine staff immediately
parents should be contacted by sports medicine staff
inform coach(es) and administration
obtain medical history and insurance information
appropriate injury reports should be completed
Emergency Telephone Numbers
Hospital
Emergency Department
University Health Center
Campus Police
-
Emergency Signals
Physician: arm extended overhead with clenched first
Paramedics: point to location in end zone by home locker room and wave onto field
Spine board: arms held horizontally
Stretcher: supinated hands in front of body or waist level
Splints: hand to lower leg or thigh
screenings, adequate medical coverage, safe practice and
training techniques, and other safety measures.1,22 However,
accidents and injuries are inherent with sports participation,
and proper preparation on the part of the sports medicine
team will enable each emergency situation to be managed
appropriately.
The goal of the sports medicine team is the delivery of the
highest possible quality health care to the athlete. Management
of the emergency situation that occurs during athletic activities
may involve certified athletic trainers and students, emergency
medical personnel, physicians, and coaches working together.
Just as with an athletic team, the sports medicine team must
work together as an efficient unit to accomplish its goals.22 In
an emergency situation, the team concept becomes even more
critical, because time is crucial and seconds may mean the
difference among life, death, and permanent disability. The
sharing of information, training, and skills among the various
emergency medical care providers helps reach the goal.22,23
Implementation. Once the importance of the emergency
plan is realized and the plan has been developed, the plan must
be implemented. Implementation of the emergency plan requires 3 basic steps.23
First, the plan must be committed to writing (Table) to provide a clear response mechanism and to allow for continuity
among emergency team members.14,16 This can be accomplished by using a flow sheet or an organizational chart. It is
also important to have a separate plan or to modify the plan
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• Number 1 • March 2002
for different athletic venues and for practices and games.
Emergency team members, such as the team physician, who
are present at games may not necessarily be present at practices. Moreover, the location and type of equipment and communication devices may differ among sports, venues, and activity levels.
The second step is education.23 It is important to educate
all the members of the emergency team regarding the emergency plan. All personnel should be familiar with the emergency medical services system that will provide coverage to
their venues and include their input in the emergency plan.
Each team member, as well as institution or organization administrators, should have a written copy of the emergency plan
that provides documentation of his or her roles and responsibilities in emergency situations. A copy of the emergency plan
specific to each venue should be posted prominently by the
available telephone.
Third, the emergency plan and procedures have to be rehearsed.16 This provides team members a chance to maintain
their emergency skills at a high level of competency. It also
provides an opportunity for athletic trainers and emergency
medical personnel to communicate regarding specific policies
and procedures in their particular region of practice.22 This
rehearsal can be accomplished through an annual in-service
meeting, preferably before the highest-risk sports season (eg,
football, ice hockey, lacrosse). Reviews should be undertaken
as needed throughout the sports season, because emergency
medical procedures and personnel may change.
Personnel. In an athletic environment, the first person who
responds to an emergency situation may vary widely22,24; it
may be a coach or a game official, a certified athletic trainer,
an emergency medical technician, or a physician. This variation in the first responder makes it imperative that an emergency plan be in place and rehearsed. With a plan in place
and rehearsed, these differently trained individuals will be able
to work together as an effective team when responding to
emergency situations.
The plan should also outline who is responsible for summoning help and clearing the uninjured from the area.
In addition, all personnel associated with practices, competitions, skills instruction, and strength and conditioning activities should have training in automatic external defibrillation
and current certification in cardiopulmonary resuscitation, first
aid, and the prevention of disease transmission.5,7
Equipment. All necessary supplemental equipment should
be at the site and quickly accessible.13,25 Equipment should be
in good operating condition, and personnel must be trained in
advance to use it properly. Improvements in technology and
emergency training require personnel to become familiar with
the use of automatic external defibrillators, oxygen, and advanced airways.
It is imperative that health professionals and organizational
administrators recognize that recent guidelines published by
the American Heart Association call for the availability and
use of automatic external defibrillators and that defibrillation
is considered a component of basic life support.26 In addition,
these guidelines emphasize use of the bag-valve mask in emergency resuscitation and the use of emergency oxygen and advanced airways in emergency care. Personnel should consider
receiving appropriate training for these devices and should
limit use to devices for which they have been trained.
To ensure that emergency equipment is in working order,
all equipment should be checked on a regular basis. Also, the
use of equipment should be regularly rehearsed by emergency
personnel, and the emergency equipment that is available
should be appropriate for the level of training of the emergency medical providers and the venue.
Communication. Access to a working telephone or other
telecommunications device, whether fixed or mobile, should
be ensured.5,17,21 The communications system should be
checked before each practice or competition to ensure proper
working order. A back-up communication plan should be in
effect in case the primary communication system fails. A listing of appropriate emergency numbers should be either posted
by the communication system or readily available, as well as
the street address of the venue and specific directions (cross
streets, landmarks, and so on) (Table).
Transportation. The emergency plan should encompass
transportation of the sick and injured. Emphasis should be
placed on having an ambulance on site at high-risk events.15
Emergency medical services response time should also be factored in when determining on-site ambulance coverage. Consideration should be given to the level of transportation service
that is available (eg, basic life support, advanced life support)
and the equipment and training level of the personnel who
staff the ambulance.23
In the event that an ambulance is on site, a location should
be designated with rapid access to the site and a cleared route
for entering and exiting the venue.19 In the emergency evaluation, the primary survey assists the emergency care provider
in identifying emergencies that require critical intervention
and in determining transport decisions. In an emergency situation, the athlete should be transported by ambulance to the
most appropriate receiving facility, where the necessary staff
and equipment can deliver appropriate care.23
In addition, a plan must be available to ensure that the activity areas are supervised if the emergency care provider
leaves the site to transport the athlete.
Venue Location. The emergency plan should be venue specific, based on the site of the practice or competition and the
activity involved (Table). The plan for each venue should encompass accessibility to emergency personnel, communication
system, equipment, and transportation.
At home sites, the host medical providers should orient the
visiting medical personnel regarding the site, emergency personnel, equipment available, and procedures associated with
the emergency plan.
At away or neutral sites, the coach or athletic trainer should
identify, before the event, the availability of communication
with emergency medical services and should verify service
and reception, particularly in rural areas. In addition, the name
and location of the nearest emergency care facility and the
availability of an ambulance at the event site should be ascertained.
Emergency Care Facilities. The emergency plan should
incorporate access to an emergency medical facility. In selection of the appropriate facility, consideration should be given
to the location with respect to the athletic venue. Consideration
should also include the level of service available at the emergency facility.
The designated emergency facility and emergency medical
services should be notified in advance of athletic events. Furthermore, it is recommended that the emergency plan be reviewed with both medical facility administrators and in-service medical staff regarding pertinent issues involved in athlete
care, such as proper removal of athletic equipment in the facility when appropriate.22,23,27
Documentation. A written emergency plan should be reviewed and approved by sports medicine team members and
institutions involved. If multiple facilities or sites are to be
used, each will require a separate plan. Additional documentation should encompass the following15,16:
1. Delineation of the person and/or group responsible for
documenting the events of the emergency situation
2. Follow-up documentation on evaluation of response to
emergency situation
3. Documentation of regular rehearsal of the emergency plan
4. Documentation of personnel training
5. Documentation of emergency equipment maintenance
It is prudent to invest organizational and institutional ownership in the emergency plan by involving administrators and
sport coaches as well as sports medicine personnel in the planning and documentation process. The emergency plan should
be reviewed at least annually with all involved personnel. Any
revisions or modifications should be reviewed and approved
by the personnel involved at all levels of the sponsoring organization or institution and of the responding emergency
medical services.
SUMMARY
The purpose of this statement is to present the position of
the NATA on emergency planning in athletics. Specifically,
Journal of Athletic Training
103
professional and legal requirements mandate that organizations
or institutions sponsoring athletic activities have a written
emergency plan. A well-thought-out emergency plan consists
of a number of factors, including, but not necessarily limited
to, personnel, equipment, communication, transportation, and
documentation. Finally, all sports medicine professionals,
coaches, and organizational administrators share professional
and legal duties to develop, implement, and evaluate emergency plans for sponsored athletic activities.
10.
11.
12.
13.
ACKNOWLEDGMENTS
14.
This position statement was reviewed for the National Athletic
Trainers’ Association by the Pronouncements Committee and by John
Cottone, EdD, ATC; Francis X. Feld, MEd, MS, CRNA, ATC,
NREMT-P; and Richard Ray, EdD, ATC.
16.
REFERENCES
17.
18.
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4. Nowlan WP, Davis GA, McDonald B. Preparing for sudden emergencies.
Athl Ther Today. 1996;1(1):45–47.
5. Shea JF. Duties of care owed to university athletes in light of Kleinecht.
J Coll Univ Law. 1995;21:591–614.
6. Halpin T, Dick RW. 1999–2000 NCAA Sports Medicine Handbook. Indianapolis, IN: National Collegiate Athletic Association; 1999.
7. Brown GT. NCAA group raising awareness on medical coverage. NCAA
News. 1999; March 15:6–7.
8. Shultz SJ, Zinder SM, Valovich TC. Sports Medicine Handbook. Indianapolis, IN: National Federation of State High School Associations;
2001.
9. Dempsey CW. Memorandum to all National Collegiate Athletic Association Institutions: Emergency Care and Coverage at NCAA Institutions.
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Indianapolis, IN: National Collegiate Athletics Association; March 25,
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National Athletic Trainers’ Association Education Council. Athletic
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National Athletic Trainers’ Association Board of Certification. Role Delineation Study of the Entry-Level Athletic Trainer Certification Examination. 3rd ed. Philadelphia, PA: FA Davis; 1995.
Herbert DL. Do you need a written emergency response plan? Sports
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Rubin A. Emergency equipment: what to keep on the sidelines. Physician
Sportsmed. 1993;21(9):47–54.
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Rankin JM, Ingersoll C. Athletic Training Management: Concepts and
Applications. St Louis, MO: Mosby-Year Book Inc; 1995:175–183.
Herbert DL. Legal Aspects of Sports Medicine. Canton, OH: Professional
Reports Corp; 1990:160–167.
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Gathers v Loyola Marymount University. Case No. C759027, Los Angeles Super Court (settled 1992).
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Hanson v Kynast, 494 NE2d 1091 (Oh 1986).
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Journal of Athletic Training 2000;35(2):212–224
© by the National Athletic Trainers’ Association, Inc
www.journalofathletictraining.org
National Athletic Trainers’ Association
Position Statement:
Fluid Replacement for Athletes
Douglas J. Casa, PhD, ATC, CSCS (Chair)*;
Lawrence E. Armstrong, PhD, FACSM*; Susan K. Hillman, MS, MA, ATC, PT†;
Scott J. Montain, PhD, FACSM‡; Ralph V. Reiff, MEd, ATC§;
Brent S.E. Rich, MD, ATC储; William O. Roberts, MD, MS, FACSM¶;
Jennifer A. Stone, MS, ATC#
*University of Connecticut, Storrs, CT; †Arizona School of Health Sciences, Phoenix, AZ; ‡US Army Research
Institute of Environmental Medicine, Natick, MA; §St. Vincent Hospital, Indianapolis, IN; 储Arizona State University,
Phoenix, AZ; ¶MinnHealth Family Physicians, White Bear Lake, MN; #US Olympic Training Center, Colorado
Springs, CO
Objective: To present recommendations to optimize the
fluid-replacement practices of athletes.
Background: Dehydration can compromise athletic performance and increase the risk of exertional heat injury. Athletes
do not voluntarily drink sufficient water to prevent dehydration
during physical activity. Drinking behavior can be modified by
education, increasing accessibility, and optimizing palatability.
However, excessive overdrinking should be avoided because it
can also compromise physical performance and health. We
provide practical recommendations regarding fluid replacement for athletes.
Recommendations: Educate athletes regarding the risks of
dehydration and overhydration on health and physical performance. Work with individual athletes to develop fluidreplacement practices that optimize hydration status before,
during, and after competition.
Key Words: athletic performance, dehydration, heat illness,
hydration protocol, hydration status, oral rehydration solution,
rehydration
D
more rapidly if the athlete enters the exercise session dehydrated. The onset of significant dehydration is preventable, or
at least modifiable, when hydration protocols are followed to
assure all athletes the most productive and the safest athletic
experience.
The purpose of this position stand is to 1) provide useful
recommendations to optimize fluid replacement for athletes, 2)
emphasize the physiologic, medical, and performance considerations associated with dehydration, and 3) identify factors
that influence optimal rehydration during and after athletic
participation.
uring exercise, evaporation is usually the primary
mechanism of heat dissipation. The evaporation of
sweat from the skin’s surface assists the body in
regulating core temperature. If the body cannot adequately
evaporate sweat from the skin’s surface, core temperature rises
rapidly. A side effect of sweating is the loss of valuable fluids
from the finite reservoir within the body, the rate being related
to exercise intensity, individual differences, environmental
conditions, acclimatization state, clothing, and baseline hydration status. Athletes whose sweat loss exceeds fluid intake
become dehydrated during activity. Therefore, a person with a
high sweat rate who undertakes intense exercise in a hot,
humid environment can rapidly become dehydrated. Dehydration of 1% to 2% of body weight begins to compromise
physiologic function and negatively influence performance.
Dehydration of greater than 3% of body weight further disturbs
physiologic function and increases an athlete’s risk of developing an exertional heat illness (ie, heat cramps, heat exhaustion, or heat stroke). This level of dehydration is common in
sports; it can be elicited in just an hour of exercise or even
Address correspondence to National Athletic Trainers’ Association,
Communications Department, 2952 Stemmons Freeway, Dallas, TX
75247.
212
Volume 35 • Number 2 • June 2000
RECOMMENDATIONS
The National Athletic Trainers’ Association (NATA) recommends the following practices regarding fluid replacement
for athletic participation:
1. Establish a hydration protocol for athletes, including a
rehydration strategy that considers the athlete’s sweat rate,
sport dynamics (eg, rest breaks, fluid access), environmental factors, acclimatization state, exercise duration, exercise intensity, and individual preferences (see Table 1 for
examples of potential outcomes).
2. A proper hydration protocol considers each sport’s unique
features. If rehydration opportunities are frequent (eg,
baseball, football, track and field), the athlete can consume
smaller volumes at a convenient pace based on sweat rate
and environmental conditions. If rehydration must occur at
specific times (eg, soccer, lacrosse, distance running), the
athlete must consume fluids to maximize hydration within
the sport’s confines and rules.
3. Fluid-replacement beverages should be easily accessible in
individual fluid containers and flavored to the athlete’s
preference. Individual containers permit easier monitoring
of fluid intake. Clear water bottles marked in 100-mL
(3.4-fl oz) increments provide visual reminders to athletes
to drink beyond thirst satiation or the typical few gulps.
Carrying water bottles or other hydration systems, when
practical, during exercise encourages greater fluid volume
ingestion.
4. Athletes should begin all exercise sessions well hydrated.
Hydration status can be approximated by athletes and
athletic trainers in several ways (Table 2). Assuming
proper hydration, pre-exercise body weight should be
relatively consistent across exercise sessions. Determine
the percentage difference between the current body weight
and the hydrated baseline body weight. Remember that
body weight is dynamic. Frequent exercise sessions can
induce nonfluid-related weight loss influenced by timing
of meals and defecation, time of day, and calories expended in exercise. The simplest method is comparison of
urine color (from a sample in a container) with a urine
color chart (Figure). Measuring urine specific gravity
(USG) with a refractometer (available for less than $150)
is less subjective than comparing urine color and also
simple to use. Urine volume is another indicator of
hydration status but inconvenient to collect and measure.
For color analysis or specific gravity, use midstream urine
collection for consistency and accuracy. Remember that
body weight changes during exercise give the best indication of hydration status. Because of urine and body weight
dynamics, measure urine before exercise and check body
weight (percentage of body weight change) before, during,
and after exercise sessions to estimate fluid balance.
5. To ensure proper pre-exercise hydration, the athlete should
consume approximately 500 to 600 mL (17 to 20 fl oz) of
water or a sports drink 2 to 3 hours before exercise and 200
to 300 mL (7 to 10 fl oz) of water or a sports drink 10 to
20 minutes before exercise.
6. Fluid replacement should approximate sweat and urine
losses and at least maintain hydration at less than 2% body
weight reduction. This generally requires 200 to 300 mL (7
to 10 fl oz) every 10 to 20 minutes. Specific individual
recommendations are calculated based on sweat rates,
sport dynamics, and individual tolerance. Maintaining
hydration status in athletes with high sweat rates, in sports
with limited fluid access, and during high-intensity exercise can be difficult, and special efforts should be made to
minimize dehydration. Dangerous hyperhydration is also a
risk if athletes drink based on published recommendations
and not according to individual needs.
7. Postexercise hydration should aim to correct any fluid loss
accumulated during the practice or event. Ideally completed within 2 hours, rehydration should contain water to
restore hydration status, carbohydrates to replenish glycogen stores, and electrolytes to speed rehydration. The
8.
9.
10.
11.
primary goal is the immediate return of physiologic
function (especially if an exercise bout will follow). When
rehydration must be rapid, the athlete should compensate
for obligatory urine losses incurred during the rehydration
process and drink about 25% to 50% more than sweat
losses to assure optimal hydration 4 to 6 hours after the
event.
Fluid temperature influences the amount consumed. While
individual differences exist, a cool beverage of 10° to
15°C (50° to 59°F) is recommended.
The Wet Bulb Globe Temperature (WBGT) should be
ascertained in hot environments. Very high relative humidity limits evaporative cooling; the air is nearly saturated with water vapor, and evaporation is minimized.
Thus, dehydration associated with high sweat losses can
induce a rapid core temperature increase due to the
inability to dissipate heat. Measuring core temperature
rectally allows the athlete’s thermal status to be accurately
determined. See the NATA position statement on heat
illnesses for expanded information on this topic.
In many situations, athletes benefit from including carbohydrates (CHOs) in their rehydration protocols. Consuming CHOs during the pre-exercise hydration session (2 to
3 hours pre-exercise), as in item 5, along with a normal
daily diet increases glycogen stores. If exercise is intense,
then consuming CHOs about 30 minutes pre-exercise may
also be beneficial. Include CHOs in the rehydration
beverage during exercise if the session lasts longer than 45
to 50 minutes or is intense. An ingestion rate of about 1
g/min (0.04 oz/min) maintains optimal carbohydrate metabolism: for example, 1 L of a 6% CHO drink per hour of
exercise. CHO concentrations greater than 8% increase the
rate of CHO delivery to the body but compromise the rate
of fluid emptying from the stomach and absorbed from the
intestine. Fruit juices, CHO gels, sodas, and some sports
drinks have CHO concentrations greater than 8% and are
not recommended during an exercise session as the sole
beverage. Athletes should consume CHOs at least 30
minutes before the normal onset of fatigue and earlier if
the environmental conditions are unusually extreme, although this may not apply for very intense short-term
exercise, which may require earlier intake of CHOs. Most
CHO forms (ie, glucose, sucrose, glucose polymers) are
suitable, and the absorption rate is maximized when
multiple forms are consumed simultaneously. Substances
to be limited include fructose (which may cause gastrointestinal distress); those to be avoided include caffeine,
alcohol (which may increase urine output and reduce fluid
retention), and carbonated beverages (which may reduce
voluntary fluid intake due to stomach fullness).
Those supervising athletes should be able to recognize the
basic signs and symptoms of dehydration: thirst, irritability, and general discomfort, followed by headache, weakness, dizziness, cramps, chills, vomiting, nausea, head or
neck heat sensations, and decreased performance. Early
diagnosis of dehydration decreases the occurrence and
severity of heat illness. A conscious, cognizant, dehydrated athlete without gastrointestinal distress can aggressively rehydrate orally, while one with mental compromise
from dehydration or gastrointestinal distress should be
transported to a medical facility for intravenous rehydration. For a complete description of heat illnesses and issues
Journal of Athletic Training
213
12.
13.
14.
15.
16.
214
related to hyperthermia, see the NATA position statement
on heat illnesses.
Inclusion of sodium chloride in fluid-replacement beverages should be considered under the following conditions:
inadequate access to meals or meals not eaten; physical
activity exceeding 4 hours in duration; or during the initial
days of hot weather. Under these conditions, adding
modest amounts of salt (0.3 to 0.7 g/L) can offset salt loss
in sweat and minimize medical events associated with
electrolyte imbalances (eg, muscle cramps, hyponatremia).
Adding a modest amount of salt (0.3 to 0.7 g/L) to all
hydration beverages would be acceptable to stimulate
thirst, increase voluntary fluid intake, and decrease the risk
of hyponatremia and should cause no harm.
Calculate each athlete’s sweat rate (sweating rate ⫽
pre-exercise body weight ⫺ postexercise body weight ⫹
fluid intake ⫺ urine volume/exercise time in hours) for a
representative range of environmental conditions, practices, and competitions (Table 3). This time-consuming
task can be made easier by weighing a large number of
athletes before an intense 1-hour practice session and then
reweighing them at the end of the 1-hour practice. Sweat
rate can now be easily calculated (do not allow rehydration
or urination during this 1 hour when sweat rate is being
determined to make the task even easier). This calculation
is the most fundamental consideration when establishing a
rehydration protocol. Average sweat rates from the scientific literature or other athletes can vary from 0.5 L/h to
more than 2.5 L/h (0.50 to 2.50 kg/h) and are not ideal to
use.
Heat acclimatization induces physiologic changes that
may alter individual fluid-replacement considerations.
First, sweat rate generally increases after 10 to 14 days of
heat exposure, requiring a greater fluid intake for a similar
bout of exercise. An athlete’s sweat rate should be reassessed after acclimatization. Second, moving from a cool
environment to a warm environment increases the overall
sweat rate for a bout of exercise. The athlete’s hydration
status must be closely monitored for the first week of
exercise in a warm environment. Third, increased sodium
intake may be warranted during the first 3 to 5 days of heat
exposure, since the increased thermal strain and associated
increased sweat rate increase the sodium lost in sweat.
Adequate sodium intake optimizes fluid palatability and
absorption during the first few days and may decrease
exercise-associated muscle cramping. After 5 to 10 days,
the sodium concentration of sweat decreases, and normal
sodium intake suffices.
All sports requiring weight classes (ie, wrestling, judo,
rowing) should mandate a check of hydration status at
weigh-in to ensure that the athlete is not dehydrated. A
USG less than or equal to 1.020 or urine color less than or
equal to 4 should be the upper range of acceptable on
weigh-in. Any procedures used to induce dramatic dehydration (eg, diuretics, rubber suits, exercising in a sauna)
are strictly prohibited.
Hyperhydration by ingesting a pre-exercise glycerol and
water beverage has equivocal support from well-controlled
studies. At this time, evidence is insufficient to endorse the
practice of hyperhydration via glycerol. Also, a risk of side
effects such as headaches and gastrointestinal distress
exists when glycerol is consumed.
Volume 35 • Number 2 • June 2000
17. Consider modifications when working with prepubescent
and adolescent athletes who exercise intensely in the heat
and may not fully comprehend the medical and performance consequences of dehydration. Focus special attention on schedules and event modification to minimize
environmental stress and maximize time for fluid replacement. Make available the most palatable beverage possible. Educate parents and coaches about rehydration and the
signs of dehydration. Monitor and remove a child from
activity promptly if signs or symptoms of dehydration
occur.
18. Large-scale event management (eg, tournaments, camps)
requires advance planning. Ample fluid and cups should
be conveniently available. With successive practice sessions during a day or over multiple days (as in most
summer sport camps), check hydration status daily before
allowing continued participation. Be aware of unhealthy
behaviors, such as eating disorders and dehydration in
weight-class sports. Use extra caution with novice and
unconditioned athletes, and remember, many athletes are
not supervised on a daily basis. If the WBGT dictates,
modify events (change game times or cancel) or change
game dynamics (insert nonroutine water breaks, shorten
game times). Recruit help from fellow athletic trainers in
local schools, student athletic trainers, and athletes from
other sports to ensure that hydration is maintained at all
venues (ie, along a road race course, on different fields
during a tournament). Be sure all assistants can communicate with the supervising athletic trainer at a central
location. For successive-day events, provide educational
materials on rehydration principles to inform athletes and
parents of this critical component of athletic performance.
19. Implementing a hydration protocol for athletes will only
succeed if athletes, coaches, athletic trainers, and team
physicians realize the importance of maintaining proper
hydration status and the steps required to accomplish this
goal. Here are the most critical components of hydration
education:
●
●
●
●
●
●
●
●
Educate athletes on the effects of dehydration on physical
performance.
Inform athletes on how to monitor hydration status.
Convince athletes to participate in their own hydration
protocols based on sweat rate, drinking preferences, and
personal responses to different fluid quantities.
Encourage coaches to mandate rehydration during practices
and competitions, just as they require other drills and
conditioning activities.
Have a scale accessible to assist athletes in monitoring
weight before, during, and after activity.
Provide the optimal oral rehydration solution (water, CHOs,
electrolytes) before, during, and after exercise.
Implement the hydration protocol during all practices and
games, and adapt it as needed.
Finally, encourage event scheduling and rule modifications
to minimize the risks associated with exercise in the heat.
BACKGROUND AND LITERATURE REVIEW
Dehydration and Exercise
Physiologic Implications. All physiologic systems in the
human body are influenced by dehydration.1,2 The degree of
Table 1. Sample Hydration Protocol Worksheet
Example A: College
Soccer, Katie (60 kg)*
Example B: High School
Basketball, Mike (80 kg)*
1) WBGT
2) Sweat rate†
3) Acclimatized
4) Length of activity
5) Intensity
6) Properly prehydrated
7) Individual container
8) Type of beverage
9) Assess hydration status
10) Available breaks
11) Amount given
28.3°C (83°F)
1.7 L/h
Yes
2 45-minute halves
Game situation (maximal)
No (began ⫺2% body weight)
Yes
5% to 7% CHO‡ solution
At halftime (with scale)
Halftime
Maximal comfortable predetermined amount
given at half time (about 700 to 1000 L)
12) End hydration status
13) Hydrated body weight
Pre-exercise body weight
Halftime body weight
Postexercise body weight
⫺4.8% body weight
60 kg
58.8 kg
57.5
57.1
21.1°C (70°F)
1.2 L/h
No
4 10-minute quarters
Game situation (maximal)
Yes
No (just cups)
5% to 7% CHO solution
No
Quarters, half, timeouts
200 mL at quarter breaks
400 mL at half time
100 mL at 1 timeout/half
Normal hydration
80 kg
80 kg
No measure
80.1 kg
Parameter to Consider
*Assumptions: Both are starters and play a full game.
†Sweat rate determined under similar parameters described in example (ie, acclimatization state, WBGT, intensity, etc) under normal game
conditions (ie, no injury timeouts, overtime, etc).
Note: Keep results on record for future reference.
‡CHO, carbohydrate.
Table 2. Indexes of Hydration Status
Condition
Well hydrated
Minimal dehydration
Significant
dehydration
Serious dehydration
% Body Weight
Change*
Urine Color
USG†
⫹1 to ⫺1
⫺1 to ⫺3
⫺3 to ⫺5
1 or 2
3 or 4
5 or 6
⬍1.010
1.010 –1.020
1.021–1.030
⬎5
⬎6
⬎1.030
*% Body weight change ⫽ [(pre-exercise body weight ⫺ postexercise
body weight)/pre-exercise body weight] ⫻ 100.
†USG, urine specific gravity.
See Figure for urine color chart and references. Please note that
obtaining a urine sample may not be possible if the athlete is seriously
dehydrated. These are physiologically independent entities, and the
numbers provided are only general guidelines.
dehydration dictates the extent of systemic compromise. Isolating the physiologic changes that contribute to decrements in
performance is difficult, as any change in 1 system (ie,
cardiovascular) influences the performance of other systems
(ie, thermoregulatory, muscular).3
The body attempts to balance endogenous heat production
and exogenous heat accumulation by heat dissipation via conduction, convection, evaporation, and radiation.4 The relative
contribution of each method depends on the ambient temperature, relative humidity, and exercise intensity. As ambient
temperature rises, conduction and convection decrease markedly, and radiation becomes nearly insignificant.4,5 Heat loss
from evaporation is the predominant heat-dissipating mechanism for the exercising athlete. In warm, humid conditions,
evaporation may account for more than 80% of heat loss. In
hot, dry conditions, evaporation may account for as much as
98% of cooling.5 If sufficient fluids are not consumed to offset
the rate of water loss via sweating, progressive dehydration
will occur. The sweating response is critical to body cooling
during exercise in the heat. Therefore, any factor that limits
evaporation (ie, high humidity, dehydration) will have pro-
found effects on physiologic function and athletic performance.
Water is the major component of the human body, accounting for approximately 73% of lean body mass.6 Body water is
distributed within and between cells and in the plasma. At rest,
approximately 30% to 35% of total body mass is intracellular
fluid, 20% to 25% is interstitial fluid, and 5% is plasma.6,7
Water movement between compartments occurs due to hydrostatic pressure and osmotic-oncotic gradients.6,7 Because sweat
is hypotonic relative to body water, the elevation of extracellular tonicity results in water movement from intracellular to
extracellular spaces.6 –9 As a consequence, all water compartments contribute to water deficit with dehydration.6,10 Most of
the resultant water deficits associated with dehydration, however, come from muscle and skin.11 The resulting hypovolemic-hyperosmolality condition is thought to precipitate many
of the physiologic consequences associated with dehydration.12
A major consequence of dehydration is an increase in core
temperature during physical activity, with core temperature
rising an additional 0.15 to 0.20°C for every 1% of body
weight lost (due to sweating) during the activity.13,14 The
added thermal strain occurs due to both impaired skin blood
flow and altered sweating responses,15–21 which is best illustrated by the delayed onset of skin vasodilation and sweating
when a dehydrated person begins to exercise.6 These thermoregulatory changes may negate the physiologic advantages
resulting from increased fitness21,22 and heat acclimatization.21,23 Additionally, heat tolerance is reduced and exercise
time to exhaustion occurs at lower core temperatures with
hypohydration.24
Accompanying the increase in thermal strain is greater
cardiovascular strain, as characterized by decreased stroke
volume, increased heart rate, increased systemic vascular
resistance, and possibly lower cardiac output and mean arterial
pressure.25–31 Similar to body temperature changes, the magnitude of cardiovascular changes is proportional to the water
Journal of Athletic Training
215
Table 3. Sample Sweat Rate Calculation*
A
B
C
D
E
F
G
H
I
J
Body Weight
Name
Kelly K.‡
Date
9/15
Before
Exercise
After
Exercise
⌬BW (C-D)
Drink Volume
Urine Volume†
Sweat Loss
(E⫹F⫺G)
Exercise
Time
Sweat Rate
(H/I)
kg
(lb/2.2)
kg
(lb/2.2)
kg
(lb/2.2)
kg
(lb/2.2)
61.7 kg
(lb/2.2)
kg
(lb/2.2)
kg
(lb/2.2)
kg
(lb/2.2)
kg
(lb/2.2)
60.3 kg
(lb/2.2)
g
(kg ⫻ 1000)
g
(kg ⫻ 1000)
g
(kg ⫻ 1000)
g
(kg ⫻ 1000)
1400 g
(kg ⫻ 1000)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
420 mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
90 mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
mL
(oz ⫻ 30)
1730 mL
(oz ⫻ 30)
min
h
min
h
min
h
min
h
90 min
1.5 h
mL/min
mL/h
mL/min
mL/h
mL/min
mL/h
mL/min
mL/h
19 mL/min
1153 mL/h
*Reprinted with permission from Murray R. Determining sweat rate. Sports Sci Exch. 1996;9(Suppl 63).
†Weight of urine should be subtracted if urine was excreted prior to postexercise body weight.
‡In the example, Kelly K. should drink about 1 L (32 oz) of fluid during each hour of activity to remain well hydrated.
deficit. For example, heart rate rises an additional 3 to 5 beats
per minute for every 1% of body weight loss.14 The strokevolume reduction seen with dehydration appears to be due to
reduced central venous pressure, resulting from reduced blood
volume and the additional hyperthermia imposed by dehydration.6,14,25,32–34
Both hypovolemia7,17,35,36 and hypertonicity7,35,37–39 have
been suggested as mechanisms for the altered thermoregulatory
and cardiovascular responses during dehydration. Manipulation of each factor independently has resulted in decreased
blood flow to the skin and sweating responses.28,34 Some
authors17,35 have argued that hypovolemia is primarily responsible for the thermoregulatory changes by reducing cardiac
preload and may alter the feedback to the hypothalamus via the
atrial pressure receptors (baroreceptors). The hypothalamic
thermoregulatory centers may induce a decrease in the blood
volume perfusing the skin in order to reestablish a normal
cardiac preload. Some studies40,41 have provided support for
this hypothesis, but it is clearly not the only variable influencing thermoregulation during hypohydration. Two hypotheses
explain the role of hyperosmolality on the thermoregulatory
system. Peripheral regulation may occur via the strong osmotic
pressure influence of the interstitium, limiting the available
fluid sources for the eccrine sweat glands.42 However, while
this peripheral influence is likely, it seems more feasible that
central brain regulation plays the largest role.7 The neurons
surrounding the thermoregulatory control centers in the hypothalamus are sensitive to osmolality.43,44 Changes in the
plasma osmolality of the blood perfusing the hypothalamus
affect body water regulation and the desire for fluid consumption.28,32,45 It is likely that both hypovolemia and hypertonicity
contribute to body fluid regulation.
Potential changes at the level of the muscle tissue include a
possible increased rate of glycogen degradation,18,46,47 elevated
muscle temperature,48 and increased lactate levels.49 These
changes may be caused by a decrease in blood perfusion of the
muscle tissue during the recovery between contractions.50
The psychological changes associated with exercise in a
dehydrated state should not be overlooked. Dehydration increases the rating of perceived exertion and impairs mental
functioning.14,51 Dehydration also decreases the motivation to
exercise and decreases the time to exhaustion, even in instances when strength is not compromised.52–54 These are
216
Volume 35 • Number 2 • June 2000
important factors when considering the motivation required by
high-level athletes to maintain maximal performance.
Performance Implications. Studies investigating the role of
dehydration on muscle strength have generally shown decrements in performance at 5% or more dehydration.15,33,55–58
The greater the degree of dehydration, the more negative the
impact on physiologic systems and overall athletic performance.
Most studies30,55,59 – 62 that address the influence of dehydration on muscle endurance show that dehydration of 3% to
4% elicits a performance decrement, but in 1 study,33 this
finding was not supported. Interestingly, hypohydrated wrestlers who were working at maximal or near-maximal muscle
activity for more than 30 seconds had a decrease in performance.63 The environmental conditions may also play an
important role in muscle endurance.33,48
The research concerning maximal aerobic power and the
physical work capacity for extended exercise is relatively consistent. Maximal aerobic power usually decreases with more than
3% hypohydration.6 In the heat, aerobic power decrements are
exaggerated.33 Even at 1% to 2% hypohydration in a cool
environment,64,65 loss of aerobic power is demonstrated. Two
important studies have noted a decrease in physical work capacity
with less than 2% dehydration during intense exercise in the
heat.66,67 When the percentage of dehydration increased, physical
work capacity decreased by as much as 35% to 48%,68 and
physical work capacity often decreased even when maximal
aerobic power did not change.46,64,65 Hypohydration of 2.5% of
body weight results in significant performance decrements while
exercising in the heat, regardless of fitness or heat acclimation
status, although enhanced fitness and acclimation can lessen the
effects of dehydration.69 Partial rehydration will enhance performance during an ensuing exercise session in the heat, which is
important when faced with the reality of sports situations.49,70 The
performance decrements noted with low to moderate levels of
hypohydration may be due to an increased perception of fatigue.50
Rehydration and Exercise
Factors Influencing Rehydration. The degree of environmental stress is determined by temperature, humidity, wind
speed, and radiant energy load, which induce physiologic
changes that affect the rehydration process.71–73 Fluid intake
increases substantially when ambient temperature rises above
25°C; the rehydration stimulus can also be psychological.74,75
An athlete exercising in the heat will voluntarily ingest more
fluid if it is chilled.76 –78 Individual differences in learned
behavior also play a role in the rehydration process.71 An
athlete who knows that rehydrating enhances subsequent performance is more apt to consume fluid before significant
dehydration occurs, so appropriate education of athletes is
essential.
The physical characteristics of the rehydration beverage can
dramatically influence fluid replacement.71,75,78 Salinity, color,
sweetness, temperature, flavor, carbonation, and viscosity all
affect how much an athlete drinks.16,75,79 – 85 Since most fluid
consumed by athletes is with meals, the presence of ample
fluid during meals and adequate amount of time to eat are
critical to rehydration.79 When access to meals is limited, a
CHO-electrolyte beverage will help maintain CHO and electrolyte intake along with hydration status.86
Other factors that contribute to fluid replacement include the
individual’s mood (calmness is associated with enhanced
rehydration) and the degree of concentration required by the
task.71 For example, industrial laborers need frequent breaks to
rehydrate because they must remain focused on a specific task.
This need for concentration may explain why many elite
mountain bikers use a convenient back-mounted hydration
system instead of the typical rack-mounted water bottle. The
back-mounted water reservoir may allow the cyclist to enhance
rehydration while remaining focused on terrain, speed, gears,
braking, and exertion.87 Accessibility to a fluid and ease of
drinking may explain why athletes consume more fluid while
cycling compared with running in a simulated duathlon.88
Hydration before Exercise. An athlete should begin exercising well hydrated. Many athletes who perform repeated
bouts of exercise on the same day or on consecutive days can
become chronically dehydrated. When a hypohydrated athlete
begins to exercise, physiologic mechanisms are compromised,64,89,90 and the extent of the dysfunction is related to the
degree of thermal stress experienced by the athlete.91 Athletes
may require substantial assistance in obtaining fluids as evidenced by the phenomena of voluntary (when individuals drink
insufficient quantities to replace fluid losses) and involuntary
dehydration.92
Athletes should ingest 500 mL of fluid 2 hours before the
event (which allows ample time to urinate excess fluid) to
ensure proper hydration and physiologic function at the onset
of exercise.79,93,94 Mandatory pre-exercise hydration is physiologically advantageous and more effective than hydration
dictated by often insufficient personal preference.95,96 Ingesting a nutritionally balanced diet and fluids during the 24 hours
before an exercise session is also crucial. Increasing CHO
intake before endurance activity may be beneficial for performance97–99 and may even enhance performance for activities
as short as 10 minutes,100 but it may have a limited effect on
resistance exercise.101
There has been recent interest in potential benefits of
purposefully overhydrating before exercise to postpone the
onset of water deficit.33,102–108 While an enhanced hydration
state is often reported with glycerol use, this does not always
translate into a performance improvement.109 A recent study110
found increased exercise time and plasma volume during
exercise to exhaustion in the heat when subjects were rehydrated with water and glycerol before exercise as compared
with rehydration using an equal volume of water without
glycerol. However, another study111 found no benefits of
glycerol ingestion when the ensuing exercise took place in a
thermoneutral environment. Hyperhydrating before exercise,
even without glycerol, may enhance thermoregulatory function112 and limit the performance decrements normally noted
with dehydration109 while exercising in the heat (WBGT ⬎
25°C). A key point is that the benefits associated with glycerol
use seem to be negated when proper hydration status is
maintained during exercise.113 However, many athletes are
unable to maintain hydration, so hyperhydration may be
beneficial in extreme conditions when fluid intake cannot
match sweat loss.
Rehydration during Exercise. Proper hydration during
exercise will influence cardiovascular function, thermoregulatory function, muscle functioning, fluid volume status, and
exercise performance. This topic has been extensively reviewed through the years, but some recent compilations are
especially notable.* Proper hydration during exercise enhances
heat dissipation (increased skin blood flow and sweating rate),
limits plasma hypertonicity, and helps sustain cardiac output.79,119,120 The enhanced evaporative cooling that can occur
(due to increased skin blood flow and maintained perfusion of
working muscles) is the result of sustained cardiac filling
pressure.26 Rehydration during exercise conserves the centrally
circulating fluid volume and allows maximal physiologic
responses to intense exercise in the heat.
Two important purposes of rehydration are to decrease the
rate of hyperthermia and to maintain athletic performance.35,121 A classic study122 showed that changes in rectal
temperature during exercise depended on the degree of fluid
intake. When water intake equaled sweat loss, rise in core
temperature was slowest when compared with ad libidum
water and no-water groups. This benefit of rehydration on
thermoregulatory function is likely due to increased blood
volume,123 reduced hyperosmolality,124 reduced cellular dehydration,125 and improved maintenance of extravascular fluid
volume.126 Some studies127,128 have not shown a physiologic
or performance benefit when rehydration occurred during a
1-hour intense exercise session in mild environmental conditions. The likely reason for a lack of benefit in these studies
was the fact that the exercise session did not elicit enough
sweat loss to cross the physiologic threshold of percentage of
body weight loss (eg, ⫺2%) that would negatively influence
performance and physiologic function. For example, in 1 of the
studies,127 the subjects had only lost 1.5% of body weight at
the completion of the exercise session.
Athletes generally do not rehydrate to pre-exercise levels
during exercise due to personal choice,75,129 fluid availability,129
the circumstances of competition,79 or a combination of these
factors. Athletes should aim to drink quantities equal to sweat and
urine losses, and while they rarely meet this goal, athletes can
readily handle these large volumes (⬎1 L/h).130 –132 Additionally,
athletes may not need to exactly match fluid intake with sweat loss
to maintain water balance given the small contribution of water
from metabolic processes.133
Appealing to individual taste preferences may encourage
athletes to drink more fluids. In addition, including CHOs
and electrolytes (especially sodium and potassium) in the
rehydration drink can maintain blood glucose, CHO oxidation, and electrolyte balance and can maintain performance
*References 6, 27, 71, 76, 79, 107, 108, 114 –118.
Journal of Athletic Training
217
if the exercise session exceeds about 50 minutes in duration.79,118,130,134 –152 Also, recent evidence153,154 indicates
that athletes performing extremely intense intermittent activity with total exercise times of less than 50 minutes may
benefit from ingestion of CHOs in the rehydration beverage.
Rates of gastric emptying and intestinal absorption should
also be considered.118,155–160 Fluid volume,161 fluid calorie
content, fluid osmolality, exercise intensity,162 environmental
stress,162 and fluid temperature107 are some of the most
important factors28 in determining the rates of gastric emptying
and small intestine absorption (the small intestine is the
primary site of fluid absorption). The single most important
variable may be the volume of fluid in the stomach.163,164
Maintaining 400 to 600 mL of fluid in the stomach (or the
maximum tolerated) will optimize gastric emptying.79 If CHOs
are included in the fluid, the concentration should be 4% to 8%.
Concentrations higher than 8% slow the rate of fluid absorption.165,166 Intense exercise (⬎80% of VO2 max) may also
decrease the rate of gastric emptying.155 Frequent ingestion
(every 15 to 20 minutes) of a moderate fluid volume (200 mL)
may be ideal, but it is not feasible in sports with extended
periods between breaks. The rates of gastric emptying and
intestinal absorption likely influence the speed of movement of
the ingested fluids into the plasma volume.167 Since the gastric
emptying and intestinal absorption rates are not compromised
with the addition of a 6% carbohydrate solution as compared
with water, fluid replacement and energy replenishment are
equally achievable.116,167–171 The rate of gastric emptying is
slowed163,172 by significant dehydration (⬎4%), which complicates rehydration and may increase gastrointestinal discomfort.163,172 Regardless, rehydration will still benefit the athlete’s hydration status.172
Rehydration during exercise is also influenced by the state of
acclimatization of the athlete. Heat acclimatization is achieved
after 5 to 10 days of training in a hot environment and will
increase sweat rate, decrease electrolyte losses in the sweat,
and allow athletes to better tolerate exercise in the heat.173,174
Heat acclimatization modestly increases rehydration needs due
to greater sweating. Fortunately, an athlete who is heat acclimatized has fewer deficits associated with dehydration175 and
tends to be a “better” voluntary drinker (ingests fluid earlier
and more often).1,34
An athlete who exercises for more than 4 hours and hydrates
excessively (well beyond sweat loss) only with water or
low-solute beverages may be susceptible to a relatively rare
condition known as symptomatic hyponatremia (also known as
water intoxication).76,108,176,177 Ultimately, the body cannot
excrete the consumed fluid rapidly enough to prevent intracellular swelling, which is sufficient to produce neuropsychological manifestations. Patients present with serum sodium levels
below 130 to 135 mmol/L, and the sequelae of hyponatremia
can result in death if not treated.177 The condition can most
likely be avoided if sodium is consumed with the rehydration
beverage and if fluid intake does not exceed sweat
losses.76,79,108
Every athlete will benefit from attempting to match intake
with sweating rate and urine losses. Individual differences exist
for gastric emptying and availability of fluids during particular
sports. Rehydration procedures should be tested in practice and
individually modified to maximize performance in competition.97,108,116,156
Rehydration after Exercise. Replenishing fluid volume178,179 and glycogen stores is critical in the recovery of
218
Volume 35 • Number 2 • June 2000
many body processes, including the cardiovascular, thermoregulatory, and metabolic activities.71,97,178,180,181
Based on volume and osmolality, the best fluid to drink after
exercise to replace the fluids that are lost via sweating may not
be water.71,182–184 Consuming water alone decreases osmolality, which limits the drive to drink and slightly increases urine
output. Including sodium in the rehydration beverage (or diet)
allows fluid volume to be better conserved and increases the
drive to drink.71,125,178,184 –186 Including CHOs in the rehydration solution may improve the rate of intestinal absorption
of sodium and water 118,178 and replenishes glycogen
stores.118,187,188 Replenishing glycogen stores can enhance
performance in subsequent exercise sessions189,190 and may
enhance immune function.191 While a normal diet commonly
restores proper electrolyte concentrations,192 many athletes are
forced to rehydrate between exercise sessions in the absence of
meals.178 In addition, some athletes’ meals are eaten as long as
6 hours after an exercise session, which may compromise
electrolyte availability during rehydration after intense exercise
in hot conditions.
While replenishing fluid to equal sweating losses is often
recommended, this formula does not replace urine losses.
Ingestion equal to 150% of weight loss resulted in optimal
rehydration 6 hours after exercise.185
Assessment of Hydration Status. Body weight changes,
urine color, subjective feelings, and thirst, among other indicators, offer cues to the need for rehydration.193 When preparing for an event, an athlete should know the sweat rate, assess
current hydration status, and develop a rehydration plan.
Determinations of sweat rate can be made.18,134 Hydration
status can be assessed by measuring body weight before and
after exercise sessions; monitoring urine color, USG, or urine
volume; or using a combination of these factors.194,195 A urine
color chart is included in this manuscript (Figure).196 The
general indexes of hydration status are provided in Table 3. A
refractometer offers a precise reading of USG and can be used
as a general indicator of hydration state. A reading of less than
1.010 reflects a well-hydrated condition, while a reading of
more than 1.020 reflects dehydration.134 Urine osmolality and
urine conductivity may also be useful tools in assessing
hydration status.197
The hydration plan should take into account the length of the
event, the individual’s sweat rate, exercise intensity, the
temperature and humidity, and the availability of fluids (is
fluid constantly available, as in cycling, or is it consumed in a
large bolus during a break?). Habits of the coach or athlete, or
both, may need to be altered in order to maximize the hydration
process. Any plan for rehydrating during competition should
be instituted and perfected during practice sessions; it should
also be individually implemented, given the large variation
among people in what constitutes a “comfortable” amount of
rehydration.198,199 A sample hydration protocol for preparing
an elite athlete for an event has been documented.200
Composition of Rehydration Fluid. During exercise, the
body uses 30 to 60 g of CHOs per hour that need to be replaced
to maintain CHO oxidation and delay the onset of glycogen
depletion fatigue.201–205 Thus, including 60 g of CHOs in 1 L
of fluid will not hinder fluid absorption and provides an
adequate supply of CHOs during or while recovering from an
exercise bout. The CHO concentration in the ideal fluidreplacement solution should be in the range of to 6% to 8%
(g/100 mL).117 The simple sugars, glucose or sucrose in simple
or polymer form, are the best additives to the replacement
fluid. Absorption is maximized if multiple forms of CHO are
ingested simultaneously (ie, fluid is absorbed more quickly
from the intestine if both glucose and fructose are present than
if only glucose is present).107,116,206 The amount of fructose in
the beverage should be limited to about 2% to 3% (2 to 3 g/100
mL of the beverage), since larger quantities may play a role in
decreasing rates of absorption and oxidation and causing
gastrointestinal distress.107,207 Ultimately, CHO composition
depends on the relative need to replace fluids or CHOs. During
events, when a high rate of fluid intake is necessary to sustain
hydration, the CHO composition should be kept low (eg, ⬍7%)
to optimize gastric emptying and fluid absorption. During
conditions when high rates of fluid replacement are not as
necessary (ie, during recovery from an exercise session, mild
environmental conditions, etc), the carbohydrate concentration
can be increased to optimize CHO delivery with minimal risk
of jeopardizing the hydration status.
Small quantities of sodium may enhance palatability and
retention, stimulate thirst, and prevent hyponatremia in a
susceptible individual.* Sodium concentration should be
approximately 0.3 to 0.7 g/L.72,80,108,157,208 Other valuable
sources of practical information concerning the composition
of rehydration beverages and rehydration in general are
available.†
Recognizing Dehydration in Athletes. The early signs and
symptoms of dehydration include thirst and general discomfort
and complaints. These are followed by flushed skin, weariness,
cramps, and apathy. At greater water deficits, dizziness,
headache, vomiting, nausea, heat sensations on the head or
neck, chills, decreased performance, and dyspnea may be
present.5,79,211,212 The degree of dehydration, the mental status,
and the general medical condition of the athlete will dictate the
mode, amount, type, and rate of rehydration. Identifying the
early signs of dehydration can limit the onset or degree of an
exertional heat illnesses.5,79,211,212 A comprehensive review of
the prevention, identification, and treatment of the exertional
heat illness can be found in the position stands by the NATA
and the American College of Sports Medicine.211,213
Event Management. Some events are conducted under
environmental conditions that are extreme and force the athlete
to reduce intensity or risk a heat illness. These hazardous heat
stresses can be avoided by scheduling athletic events during the
coolest part of the day or a cooler time of the year.211,214 The
reality of sport administration is that many events take place
regardless of the environmental conditions. Individuals supervising an event in a hot humid environment must ensure that
athletes have ample access to fluids, are encouraged to match
fluid intakes with sweat losses, and are monitored for dehydration and exertional heat illness. Whenever possible, minimize the exercise intensity of athletes in the extreme heat, since
this is the largest contributor to dehydration and heat illness.
When successive exercise sessions occur on the same day or on
ensuing days, hydration status, sleep, meals, and other factors
that maximize performance and enhance safety should be
maintained. Given the variety of events an athletic trainer may
supervise, we cannot formulate an event management recommendation for all sports. However, the general concepts are
interchangeable across sports and venues. For example, game
modifications such as decreasing the length of play or inserting
*References 38, 80, 108, 131, 157, 185, 208.
†References 18, 76, 107, 118, 156, 159, 160, 168, 178, 205, 209, 210.
nontraditional water breaks (especially in youth sports and
practice situations) will reduce the rate of heat illness. Closely
monitoring environmental conditions via the WBGT or the
heat index will allow an informed approach to hydration and
sweat modification. Athletes who are educated on how to
prevent and recognize dehydration are empowered to participate actively in implementing their own hydration protocols,
thereby enhancing both performance and safety. The person
responsible for the medical supervision of an event should have
a detailed plan to address facilities, equipment, supplies,
staffing, communication systems, education, and implementation of event policy.213,215–220
ACKNOWLEDGMENTS
This position statement was reviewed for the NATA by the Pronouncements Committee and reviewers Kristine L. Clark, PhD, RD,
David Lamb, PhD, and Jack Ransone, PhD, ATC.
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Journal of Athletic Training
2002;37(3):329–343
q by the National Athletic Trainers’ Association, Inc
www.journalofathletictraining.org
National Athletic Trainers’ Association
Position Statement: Exertional Heat
Illnesses
Helen M. Binkley*; Joseph Beckett†; Douglas J. Casa‡;
Douglas M. Kleiner§; Paul E. Plummer\
*Mesa State College, Grand Junction, CO; †University of Charleston, Charleston, WV; ‡University of Connecticut,
Storrs, CT; §University of Florida, Jacksonville, FL; \Indiana State University, Terre Haute, IN
Helen M. Binkley, PhD, ATC, CSCS*D, NSCA-CPT (Chair), contributed to conception and design; acquisition of the data; and
drafting, critical revision, and final approval of the article. Joseph Beckett, EdD, ATC, contributed to acquisition of the data and
drafting, critical revision, and final approval of the article. Douglas J. Casa, PhD, ATC, FACSM, contributed to conception and
design; acquisition of the data; and drafting, critical revision, and final approval of the article. Douglas M. Kleiner, PhD, ATC,
FACSM, and Paul E. Plummer, MA, ATC, contributed to acquisition of the data and drafting, critical revision, and final approval
of the article.
Address correspondence to National Athletic Trainers’ Association, Communications Department, 2952 Stemmons Freeway,
Dallas, TX 75247.
Objective: To present recommendations for the prevention,
recognition, and treatment of exertional heat illnesses and to
describe the relevant physiology of thermoregulation.
Background: Certified athletic trainers evaluate and treat
heat-related injuries during athletic activity in ‘‘safe’’ and highrisk environments. While the recognition of heat illness has improved, the subtle signs and symptoms associated with heat
illness are often overlooked, resulting in more serious problems
for affected athletes. The recommendations presented here
provide athletic trainers and allied health providers with an integrated scientific and practical approach to the prevention, recognition, and treatment of heat illnesses. These recommendations can be modified based on the environmental conditions
of the site, the specific sport, and individual considerations to
maximize safety and performance.
Recommendations: Certified athletic trainers and other allied health providers should use these recommendations to establish on-site emergency plans for their venues and athletes.
The primary goal of athlete safety is addressed through the
prevention and recognition of heat-related illnesses and a welldeveloped plan to evaluate and treat affected athletes. Even
with a heat-illness prevention plan that includes medical screening, acclimatization, conditioning, environmental monitoring,
and suitable practice adjustments, heat illness can and does
occur. Athletic trainers and other allied health providers must
be prepared to respond in an expedient manner to alleviate
symptoms and minimize morbidity and mortality.
Key Words: heat cramps, heat syncope, heat exhaustion,
heat stroke, hyponatremia, dehydration, exercise, heat tolerance
H
letes with heat illnesses, (4) determine appropriate return-toplay procedures, (5) understand thermoregulation and physiologic responses to heat, and (6) recognize groups with special
concerns related to heat exposure.
eat illness is inherent to physical activity and its incidence increases with rising ambient temperature and
relative humidity. Athletes who begin training in the
late summer (eg, football, soccer, and cross-country athletes)
experience exertional heat-related illness more often than athletes who begin training during the winter and spring.1–5 Although the hot conditions associated with late summer provide
a simple explanation for this difference, we need to understand
what makes certain athletes more susceptible and how these
illnesses can be prevented.
PURPOSE
This position statement provides recommendations that will
enable certified athletic trainers (ATCs) and other allied health
providers to (1) identify and implement preventive strategies
that can reduce heat-related illnesses in sports, (2) characterize
factors associated with the early detection of heat illness, (3)
provide on-site first aid and emergency management of ath-
ORGANIZATION
This position statement is organized as follows:
1. Definitions of exertional heat illnesses, including exerciseassociated muscle (heat) cramps, heat syncope, exercise
(heat) exhaustion, exertional heat stroke, and exertional hyponatremia;
2. Recommendations for the prevention, recognition, and
treatment of exertional heat illnesses;
3. Background and literature review of the diagnosis of exertional heat illnesses; risk factors; predisposing medical
conditions; environmental risk factors; thermoregulation,
heat acclimatization, cumulative dehydration, and cooling
therapies;
Journal of Athletic Training
329
Table 1. Signs and Symptoms of Exertional Heat Illnesses
Table 1. Continued
Condition
Sign or Symptom*
Exercise-associated muscle (heat) cramps6,9–11
Dehydration
Thirst
Sweating
Transient muscle cramps
Fatigue
Heat syncope10,12
Dehydration
Fatigue
Tunnel vision
Pale or sweaty skin
Decreased pulse rate
Dizziness
Lightheadedness
Fainting
Exercise (heat) exhaustion6,9,10,13
Normal or elevated body-core temperature
Dehydration
Dizziness
Lightheadedness
Syncope
Headache
Nausea
Anorexia
Diarrhea
Decreased urine output
Persistent muscle cramps
Pallor
Profuse sweating
Chills
Cool, clammy skin
Intestinal cramps
Urge to defecate
Weakness
Hyperventilation
Exertional heat stroke6,9,10,14
High body-core temperature (.408C [1048F])
Central nervous system changes
Dizziness
Drowsiness
Irrational behavior
Confusion
Irritability
Emotional instability
Hysteria
Apathy
Aggressiveness
Delirium
Disorientation
Staggering
Seizures
Loss of consciousness
Coma
Dehydration
Weakness
Hot and wet or dry skin
Tachycardia (100 to 120 beats per minute)
Hypotension
Hyperventilation
Vomiting
Diarrhea
Exertional hyponatremia15–18
Body-core temperature ,408C (1048F)
Nausea
Vomiting
330
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• Number 3 • September 2002
Condition
Sign or Symptom*
Extremity (hands and feet) swelling
Low blood-sodium level
Progressive headache
Confusion
Significant mental compromise
Lethargy
Altered consciousness
Apathy
Pulmonary edema
Cerebral edema
Seizures
Coma
*Not every patient will present with all the signs and symptoms for the
suspected condition.
4. Special concerns regarding exertional heat illnesses in prepubescent athletes, older athletes, and athletes with spinalcord injuries;
5. Hospitalization and recovery from exertional heat stroke
and resumption of activity after heat-related collapse; and
6. Conclusions.
DEFINITIONS OF EXERTIONAL HEAT ILLNESSES
The traditional classification of heat illness defines 3 categories: heat cramps, heat exhaustion, and heat stroke.6–8 However, this classification scheme omits several other heat- and
activity-related illnesses, including heat syncope and exertional hyponatremia. The signs and symptoms of the exertional
heat illnesses are listed in Table 1.
Heat illness is more likely in hot, humid weather but can
occur in the absence of hot and humid conditions.
Exercise-Associated Muscle (Heat) Cramps
Exercise-associated muscle (heat) cramps represent a condition that presents during or after intense exercise sessions as
an acute, painful, involuntary muscle contraction. Proposed
causes include fluid deficiencies (dehydration), electrolyte imbalances, neuromuscular fatigue, or any combination of these
factors.6,9–11,19
Heat Syncope
Heat syncope, or orthostatic dizziness, can occur when a
person is exposed to high environmental temperatures.19 This
condition is attributed to peripheral vasodilation, postural
pooling of blood, diminished venous return, dehydration, reduction in cardiac output, and cerebral ischemia.10,19 Heat syncope usually occurs during the first 5 days of acclimatization,
before the blood volume expands,12 or in persons with heart
disease or those taking diuretics.10 It often occurs after standing for long periods of time, immediately after cessation of
activity, or after rapid assumption of upright posture after resting or being seated.
Exercise (Heat) Exhaustion
Exercise (heat) exhaustion is the inability to continue exercise
associated with any combination of heavy sweating, dehydra-
tion, sodium loss, and energy depletion. It occurs most frequently in hot, humid conditions. At its worst, it is difficult to
distinguish from exertional heat stroke without measuring rectal
temperature. Other signs and symptoms include pallor, persistent muscular cramps, urge to defecate, weakness, fainting, dizziness, headache, hyperventilation, nausea, anorexia, diarrhea,
decreased urine output, and a body-core temperature that generally ranges between 368C (978F) and 408C (1048F).6,9,10,13,19
Exertional Heat Stroke
Exertional heat stroke is an elevated core temperature (usually .408C [1048F]) associated with signs of organ system
failure due to hyperthermia. The central nervous system neurologic changes are often the first marker of exertional heat
stroke. Exertional heat stroke occurs when the temperature
regulation system is overwhelmed due to excessive endogenous heat production or inhibited heat loss in challenging environmental conditions20 and can progress to complete thermoregulatory system failure. 19,21 This condition is life
threatening and can be fatal unless promptly recognized and
treated. Signs and symptoms include tachycardia, hypotension,
sweating (although skin may be wet or dry at the time of
collapse), hyperventilation, altered mental status, vomiting, diarrhea, seizures, and coma.6,10,14 The risk of morbidity and
mortality is greater the longer an athlete’s body temperature
remains above 418C (1068F) and is significantly reduced if
body temperature is lowered rapidly.22–24
Unlike classic heat stroke, which typically involves prolonged heat exposure in infants, elderly persons, or unhealthy,
sedentary adults in whom body heat-regulation mechanisms
are inefficient,25–27 exertional heat stroke occurs during physical activity.28 The pathophysiology of exertional heat stroke
is due to the overheating of organ tissues that may induce
malfunction of the temperature-control center in the brain, circulatory failure, or endotoxemia (or a combination of
these).29,30 Severe lactic acidosis (accumulation of lactic acid
in the blood), hyperkalemia (excessive potassium in the
blood), acute renal failure, rhabdomyolysis (destruction of
skeletal muscle that may be associated with strenuous exercise), and disseminated intravascular coagulation (a bleeding
disorder characterized by diffuse blood coagulation), among
other medical conditions, may result from exertional heat
stroke and often cause death.25
Exertional Hyponatremia
Exertional hyponatremia is a relatively rare condition defined as a serum-sodium level less than 130 mmol/L. Low
serum-sodium levels usually occur when activity exceeds 4
hours.19 Two, often-additive mechanisms are proposed: an athlete ingests water or low-solute beverages well beyond sweat
losses (also known as water intoxication), or an athlete’s sweat
sodium losses are not adequately replaced.15–18 The low
blood-sodium levels are the result of a combination of excessive fluid intake and inappropriate body water retention in the
water-intoxication model and insufficient fluid intake and inadequate sodium replacement in the latter. Ultimately, the intravascular and extracellular fluid has a lower solute load than
the intracellular fluids, and water flows into the cells, producing intracellular swelling that causes potentially fatal neurologic and physiologic dysfunction. Affected athletes present
with a combination of disorientation, altered mental status,
headache, vomiting, lethargy, and swelling of the extremities
(hands and feet), pulmonary edema, cerebral edema, and seizures. Exertional hyponatremia can result in death if not treated properly. This condition can be prevented by matching fluid
intake with sweat and urine losses and by rehydrating with
fluids that contain sufficient sodium.31,32
RECOMMENDATIONS
The National Athletic Trainers’ Association (NATA) advocates the following prevention, recognition, and treatment
strategies for exertional heat illnesses. These recommendations
are presented to help ATCs and other allied health providers
maximize health, safety, and sport performance as they relate
to these illnesses. Athletes’ individual responses to physiologic
stimuli and environmental conditions vary widely. These recommendations do not guarantee full protection from heat-related illness but should decrease the risk during athletic participation. These recommendations should be considered by
ATCs and allied health providers who work with athletes at
risk for exertional heat illnesses to improve prevention strategies and ensure proper treatment.
Prevention
1. Ensure that appropriate medical care is available and that
rescue personnel are familiar with exertional heat illness prevention, recognition, and treatment. Table 2 provides general
guidelines that should be considered.7 Ensure that ATCs and
other health care providers attending practices or events are
allowed to evaluate and examine any athlete who displays
signs or symptoms of heat illness33,34 and have the authority
to restrict the athlete from participating if heat illness is present.
2. Conduct a thorough, physician-supervised, preparticipation
medical screening before the season starts to identify athletes
predisposed to heat illness on the basis of risk factors34–36 and
those who have a history of exertional heat illness.
3. Adapt athletes to exercise in the heat (acclimatization)
gradually over 10 to 14 days. Progressively increase the intensity and duration of work in the heat with a combination
of strenuous interval training and continuous exercise.6,9,14,33,37–44 Well-acclimatized athletes should train for 1
to 2 hours under the same heat conditions that will be present
for their event.6,45,46 In a cooler environment, an athlete can
wear additional clothing during training to induce or maintain
heat acclimatization. Athletes should maintain proper hydration during the heat-acclimatization process.47
4. Educate athletes and coaches regarding the prevention,
recognition, and treatment of heat illnesses9,33,38,39,42,48–51 and
the risks associated with exercising in hot, humid environmental conditions.
5. Educate athletes to match fluid intake with sweat and
urine losses to maintain adequate hydration.* (See the ‘‘National Athletic Trainers’ Association Position Statement: Fluid
Replacement in Athletes.’’52) Instruct athletes to drink sodiumcontaining fluids to keep their urine clear to light yellow to
improve hydration33,34,52–55 and to replace fluids between
practices on the same day and on successive days to maintain
less than 2% body-weight change. These strategies will lessen
the risk of acute and chronic dehydration and decrease the risk
of heat-related events.
*References 9, 29, 37, 38, 40, 41, 43, 52–66.
Journal of Athletic Training
331
Table 2. Prevention Checklist for the Certified Athletic Trainer*
1. Pre-event preparation
Am I challenging unsafe rules (eg, ability to receive fluids, modify game and practice times)?
Am I encouraging athletes to drink before the onset of thirst and to be well hydrated at the start of activity?
Am I familiar with which athletes have a history of a heat illness?
Am I discouraging alcohol, caffeine, and drug use?
Am I encouraging proper conditioning and acclimatization procedures?
2. Checking hydration status
Do I know the preexercise weight of the athletes (especially those at high risk) with whom I work, particularly during hot and humid
conditions?
Are the athletes familiar with how to assess urine color? Is a urine color chart accessible?
Do the athletes know their sweat rates and, therefore, know how much to drink during exercise?
Is a refractometer or urine color chart present to provide additional information regarding hydration status in high-risk athletes when
baseline body weights are checked?
3. Environmental assessment
Am I regularly checking the wet-bulb globe temperature or temperature and humidity during the day?
Am I knowledgeable about the risk categories of a heat illness based on the environmental conditions?
Are alternate plans made in case risky conditions force rescheduling of events or practices?
4. Coaches’ and athletes’ responsibilities
Are coaches and athletes educated about the signs and symptoms of heat illnesses?
Am I double checking to make sure coaches are allowing ample rest and rehydration breaks?
Are modifications being made to reduce risk in the heat (eg, decrease intensity, change practice times, allow more frequent breaks,
eliminate double sessions, reduce or change equipment or clothing requirements, etc)?
Are rapid weight-loss practices in weight-class sports adamantly disallowed?
5. Event management
Have I checked to make sure proper amounts of fluids will be available and accessible?
Are carbohydrate-electrolyte drinks available at events and practices (especially during twice-a-day practices and those that last longer
than 50 to 60 minutes or are extremely intense in nature)?
Am I aware of the factors that may increase the likelihood of a heat illness?
Am I promptly rehydrating athletes to preexercise weight after an exercise session?
Are shaded or indoor areas used for practices or breaks when possible to minimize thermal strain?
6. Treatment considerations
Am I familiar with the most common early signs and symptoms of heat illnesses?
Do I have the proper field equipment and skills to assess a heat illness?
Is an emergency plan in place in case an immediate evacuation is needed?
Is a kiddy pool available in situations of high risk to initiate immediate cold-water immersion of heat-stroke patients?
Are ice bags available for immediate cooling when cold-water immersion is not possible?
Have shaded, air-conditioned, and cool areas been identified to use when athletes need to cool down, recover, or receive treatment?
Are fans available to assist evaporation when cooling?
Am I properly equipped to assess high core temperature (ie, rectal thermometer)?
7. Other situation-specific considerations
*Adapted with permission from Casa.7
Table 3. Wet-Bulb Globe Temperature Risk Chart62–67*
WBGT
Flag Color
Level of Risk
Comments
,188C (,658F)
18–238C (65–738F)
Green
Yellow
Low
Moderate
23–288C (73–828F)
Red
High
.288C (828F)
Black
Extreme or hazardous
Risk low but still exists on the basis of risk factors
Risk level increases as event progresses through the
day
Everyone should be aware of injury potential; individuals at risk should not compete
Consider rescheduling or delaying the event until safer
conditions prevail; if the event must take place, be
on high alert
*Adapted with permission from Roberts.67
6. Encourage athletes to sleep at least 6 to 8 hours at night
in a cool environment,41,35,50 eat a well-balanced diet that follows the Food Guide Pyramid and United States Dietary
Guidelines,56–58 and maintain proper hydration status. Athletes
exercising in hot conditions (especially during twice-a-day
practices) require extra sodium from the diet or rehydration
beverages or both.
7. Develop event and practice guidelines for hot, humid
weather that anticipate potential problems encountered based
332
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• Number 3 • September 2002
on the wet-bulb globe temperature (WBGT) (Table 3) or heat
and humidity as measured by a sling psychrometer (Figure 1),
the number of participants, the nature of the activity, and other
predisposing risk factors.14,51 If the WBGT is greater than
288C (828F, or ‘‘very high’’ as indicated in Table 3, Figure 1),
an athletic event should be delayed, rescheduled, or moved
into an air-conditioned space, if possible.69–74 It is important
to note that these measures are based on the risk of environmental stress for athletes wearing shorts and a T-shirt; if an
Figure 1. Risk of heat exhaustion or heat stroke while racing in hot
environments. However, Figure 2 may be better suited for estimating heat-stroke risk when equipment is worn. Reprinted with permission from Convertino VA, Armstrong LE, Coyle EF, et al. American College of Sports Medicine position stand: exercise and fluid
replacement. Med Sci Sports Exerc. 1996;28:i–vii.31
athlete is wearing additional clothing (ie, football uniform,
wetsuit, helmet), a lower WBGT value could result in comparable risk of environmental heat stress (Figure 2).75,76 If the
event or practice is conducted in hot, humid conditions, then
use extreme caution in monitoring the athletes and be proactive in taking preventive steps. In addition, be sure that emergency supplies and equipment are easily accessible and in
good working order. The most important factors are to limit
intensity and duration of activity, limit the amount of clothing
and equipment worn, increase the number and length of rest
breaks, and encourage proper hydration.
Modify activity under high-risk conditions to prevent exertional heat illnesses.19,21 Identify individuals who are susceptible to heat illnesses. In some athletes, the prodromal signs
and symptoms of heat illnesses are not evident before collapse,
but in many cases, adept medical supervision will allow early
intervention.
8. Check the environmental conditions before and during
the activity, and adjust the practice schedule accordingly.29,38,41,42,60 Schedule training sessions to avoid the hottest
part of the day (10 AM to 5 PM) and to avoid radiant heating
from direct sunlight, especially in the acclimatization during
the first few days of practice sessions.9,29,33,34,38,40,50,60
9. Plan rest breaks to match the environmental conditions and
the intensity of the activity.33,34 Exercise intensity and environmental conditions should be the major determinants in deciding
the length and frequency of rest breaks. If possible, cancel or
postpone the activity or move it indoors (if air conditioned) if
the conditions are ‘‘extreme or hazardous’’ (see Table 3) or
‘‘very high’’ (see Figure 1) or to the right of the circled line
(see Figure 2). General guidelines during intense exercise would
include a work:rest ratio of 1:1, 2:1, 3:1, and 4:1 for ‘‘extreme
or hazardous’’ (see Table 3) or ‘‘very high’’ (see Figure 1),
‘‘high,’’ ‘‘moderate,’’ or ‘‘low’’ environmental risk, respectively.41,77 For activities such as football in which equipment must
be considered, please refer to Figure 2 for equipment modifications and appropriate work:rest ratios for various environmental conditions. Rest breaks should occur in the shade if possible, and hydration during rest breaks should be encouraged.
Figure 2. Heat stress risk temperature and humidity graph. Heatstroke risk rises with increasing heat and relative humidity. Fluid
breaks should be scheduled for all practices and scheduled more
frequently as the heat stress rises. Add 58 to temperature between
10 AM and 4 PM from mid May to mid September on bright, sunny
days. Practices should be modified for the safety of the athletes
to reflect the heat-stress conditions. Regular practices with full
practice gear can be conducted for conditions that plot to the left
of the triangles. Cancel all practices when the temperature and
relative humidity plot is to the right of the circles; practices may
be moved into air-conditioned spaces or held as walk-through sessions with no conditioning activities.
Conditions that plot between squares and circles: increase restto-work ratio with 5- to 10-minute rest and fluid breaks every 15 to
20 minutes; practice should be in shorts only with all protective
equipment removed.
Conditions that plot between triangles and squares: increase
rest-to-work ratio with 5- to 10-minute rest and fluid breaks every
20 to 30 minutes; practice should be in shorts with helmets and
shoulder pads (not full equipment).
Adapted with permission from Kulka J, Kenney WL. Heat balance
limits in football uniforms: how different uniform ensembles alter
the equation. Physician Sportsmed. 2002;30(7):29–39.68
10. Implement rest periods at mealtime by allowing 2 to 3
hours for food, fluids, nutrients, and electrolytes (sodium and
potassium) to move into the small intestine and bloodstream
before the next practice.34,50,77
11. Provide an adequate supply of proper fluids (water or
sports drinks) to maintain hydration9,34,38,40,50,60 and institute
a hydration protocol that allows the maintenance of hydration
status.34,49 Fluids should be readily available and served in
containers that allow adequate volumes to be ingested with
ease and with minimal interruption of exercise.49,52 The goal
should be to lose no more than 2% to 3% of body weight during
the practice session (due to sweat and urine losses).78–82 (See
the ‘‘National Athletic Trainers’ Association Position Statement: Fluid Replacement in Athletes.’’52)
12. Weigh high-risk athletes (in high-risk conditions, weigh
all athletes) before and after practice to estimate the amount
of body water lost during practice and to ensure a return to
prepractice weight before the next practice. Following exercise
athletes should consume approximately 1–1.25 L (16 oz) of
fluid for each kilogram of body water lost during exercise.†
†References 6, 9, 29, 33, 38, 40, 49, 60, 77, 83.
Journal of Athletic Training
333
13. Minimize the amount of equipment and clothing worn
by the athlete in hot or humid (or both) conditions. For example, a full football uniform prevents sweat evaporation from
more than 60% of the body.29,33,40,51,77 Consult Figure 2 for
possible equipment and clothing recommendations. When athletes exercise in the heat, they should wear loose-fitting, absorbent, and light-colored clothing; mesh clothing and newgeneration cloth blends have been specially designed to allow
more effective cooling.‡
14. Minimize warm-up time when feasible, and conduct
warm-up sessions in the shade when possible to minimize the
radiant heat load in ‘‘high’’ or ‘‘very high’’ or ‘‘extreme or
hazardous’’ (see Table 3, Figure 1) conditions.77
15. Allow athletes to practice in shaded areas and use electric or cooling fans to circulate air whenever feasible.66
16. Include the following supplies on the field, in the locker
room, and at various other stations:
• A supply of cool water or sports drinks or both to meet the
participants’ needs (see the ‘‘National Athletic Trainers’ Association Position Statement: Fluid Replacement in Athletes’’52 for recommendations regarding the appropriate
composition of rehydration beverages based on the length
and intensity of the activity)29,34,38
• Ice for active cooling (ice bags, tub cooling) and to keep
beverages cool during exercise29,38
• Rectal thermometer to assess body-core temperature39,74,75,87,88
• Telephone or 2-way radio to communicate with medical personnel and to summon emergency medical transportation38,39,48
• Tub, wading pool, kiddy pool, or whirlpool to cool the trunk
and extremities for immersion cooling therapy35,65
17. Notify local hospital and emergency personnel before
mass participation events to inform them of the event and the
increased possibility of heat-related illnesses.41,89
18. Mandate a check of hydration status at weigh-in to ensure athletes in sports requiring weight classes (eg, wrestling,
judo, rowing) are not dehydrated. Any procedures used to induce dramatic dehydration (eg, diuretics, rubber suits, exercising in a sauna) are strictly prohibited.52 Dehydrated athletes
exercising at the same intensity as euhydrated athletes are at
increased risk for thermoregulatory strain (see the ‘‘National
Athletic Trainers’ Association Position Statement: Fluid Replacement in Athletes’’52).
Recognition and Treatment
19. Exercise-associated muscle (heat) cramps:
• An athlete showing signs or symptoms including dehydration, thirst, sweating, transient muscle cramps, and fatigue
is likely experiencing exercise-associated muscle (heat)
cramps.
• To relieve muscle spasms, the athlete should stop activity,
replace lost fluids with sodium-containing fluids, and begin
mild stretching with massage of the muscle spasm.
• Fluid absorption is enhanced with sports drinks that contain
sodium.52,60,87 A high-sodium sports product may be added
to the rehydration beverage to prevent or relieve cramping
in athletes who lose large amounts of sodium in their
sweat.19 A simple salted fluid consists of two 10-grain salt
‡References 8, 9, 29, 33, 38, 40, 53, 59, 84–86.
334
Volume 37
• Number 3 • September 2002
tablets dissolved in 1 L (34 oz) of water. Intravenous fluids
may be required if nausea or vomiting limits oral fluid intake; these must be ordered by a physician.6,7,52,90,91
• A recumbent position may allow more rapid redistribution
of blood flow to cramping leg muscles.
20. Heat syncope:
• If an athlete experiences a brief episode of fainting associated with dizziness, tunnel vision, pale or sweaty skin, and
a decreased pulse rate but has a normal rectal temperature
(for exercise, 368C to 408C [978F to 1048F]), then heat syncope is most likely the cause.19
• Move the athlete to a shaded area, monitor vital signs, elevate the legs above the level of the head, and rehydrate.
21. Exercise (heat) exhaustion:
• Cognitive changes are usually minimal, but assess central
nervous system function for bizarre behavior, hallucinations,
altered mental status, confusion, disorientation, or coma (see
Table 1) to rule out more serious conditions.
• If feasible, measure body-core temperature (rectal temperature) and assess cognitive function (see Table 1) and vital
signs.19 Rectal temperature is the most accurate method possible in the field to monitor body-core temperature.34,74,75,87,88 The ATC should not rely on the oral, tympanic, or axillary temperature for athletes because these are
inaccurate and ineffective measures of body-core temperature during and after exercise.75,89,92
• If the athlete’s temperature is elevated, remove his or her
excess clothing to increase the evaporative surface and to
facilitate cooling.6,93
• Cool the athlete with fans,94 ice towels,29,38 or ice bags because these may help the athlete with a temperature of more
than 38.88C (1028F) to feel better faster.
• Remove the athlete to a cool or shaded environment if possible.
• Start fluid replacement.6,52,93,95
• Transfer care to a physician if intravenous fluids are needed6,52,90,91,96 or if recovery is not rapid and uneventful.
22. Exertional heat stroke:
• Measure the rectal temperature if feasible to differentiate between heat exhaustion and heat stroke. With heat stroke, rectal temperature is elevated (generally higher than 408C
[1048F]).19
• Assess cognitive function, which is markedly altered in exertional heat stroke (see Table 1).
• Lower the body-core temperature as quickly as possible.34,70,77 The fastest way to decrease body temperature is
to remove clothes and equipment and immerse the body
(trunk and extremities) into a pool or tub of cold water (approximately 18C to 158C [358F to 598F]).32,91,92,97–99 Aggressive cooling is the most critical factor in the treatment
of exertional heat stroke. Circulation of the tub water may
enhance cooling.
• Monitor the temperature during the cooling therapy and recovery (every 5 to 10 minutes).39,87 Once the athlete’s rectal
temperature reaches approximately 38.38C to 38.98C (1018F
to 1028F), he or she should be removed from the pool or
tub to avoid overcooling.40,100
• If a physician is present to manage the athlete’s medical care
on site, then initial transportation to a medical facility may
not be necessary so immersion can continue uninterrupted.
•
•
•
•
•
If a physician is not present, aggressive first-aid cooling
should be initiated on site and continued during emergency
medical system transport and at the hospital until the athlete
is normothermic.
Activate the emergency medical system.
Monitor the athlete’s vital signs and other signs and symptoms of heat stroke (see Table 1).34,95
During transport and when immersion is not feasible, other
methods can be used to reduce body temperature: removing
the clothing; sponging down the athlete with cool water and
applying cold towels; applying ice bags to as much of the
body as possible, especially the major vessels in the armpit,
groin, and neck; providing shade; and fanning the body with
air.39,95
In addition to cooling therapies, first-aid emergency procedures for heat stroke may include airway management. Also
a physician may decide to begin intravenous fluid replacement.87
Monitor for organ-system complications for at least 24
hours.
23. Exertional hyponatremia:
• Attempt to differentiate between hyponatremia and heat exhaustion. Hyponatremia is characterized by increasing headache, significant mental compromise, altered consciousness,
seizures, lethargy, and swelling in the extremities. The athlete may be dehydrated, normally hydrated, or overhydrated.19
• Attempt to differentiate between hyponatremia and heat
stroke. In hyponatremia, hyperthermia is likely to be less
(rectal temperature less than 408C [1048F]).19 The plasmasodium level is less than 130 mEq/L and can be measured
with a sodium analyzer on site if the device is available.
• If hyponatremia is suspected, immediate transfer to an emergency medical center via the emergency medical system is
indicated. An intravenous line should be placed to administer
medication as needed to increase sodium levels, induce diuresis, and control seizures.
• An athlete with suspected hyponatremia should not be administered fluids until a physician is consulted.
24. Return to activity
In cases of exercise-associated muscle (heat) cramps or heat
syncope, the ATC should discuss the athlete’s case with the
supervising physician. The cases of athletes with heat exhaustion who were not transferred to the physician’s care should
also be discussed with the physician. After exertional heat
stroke or exertional hyponatremia, the athlete must be cleared
by a physician before returning to athletic participation.92 The
return to full activity should be gradual and monitored.8,87
BACKGROUND AND LITERATURE REVIEW
Diagnosis
To differentiate heat illnesses in athletes, ATCs and other
on-site health care providers must be familiar with the signs
and symptoms of each condition (see Table 1). Other medical
conditions (eg, asthma, status epilepticus, drug toxicities) may
also present with similar signs and symptoms. It is important
to realize, however, that an athlete with a heat illness will not
exhibit all the signs and symptoms of a specific condition,
increasing the need for diligent observation during athletic activity.
Nonenvironmental Risk Factors
Athletic trainers and other health care providers should be
sensitive to the following nonenvironmental risk factors,
which could place athletes at risk for heat illness.
Dehydration. Sweating, inadequate fluid intake, vomiting,
diarrhea, certain medications,89,101–103 and alcohol104,105 or
caffeine106 use can lead to fluid deficit. Body-weight change
is the preferred method to monitor for dehydration in the field,
but a clinical refractometer is another accurate method (specific gravity should be no more than 1.020).34,49,107–110 Dehydration can also be identified by monitoring urine color or
body-weight changes before, during, and after a practice or an
event and across successive days.53,54
The signs and symptoms of dehydration are thirst, general
discomfort, flushed skin, weariness, cramps, apathy, dizziness,
headache, vomiting, nausea, heat sensations on the head or
neck, chills, decreased performance, and dyspnea.52 Water loss
that is not regained by the next practice increases the risk for
heat illness.110
Barriers to Evaporation. Athletic equipment and rubber or
plastic suits used for ‘‘weight loss’’ do not allow water vapor
to pass through and inhibit evaporative, convective, and radiant heat loss.111,112 Participants who wear equipment that does
not allow for heat dissipation are at an increased risk for heat
illness.113 Helmets are also limiting because a significant
amount of heat is dissipated through the head.
Illness. Athletes who are currently or were recently ill may
be at an increased risk for heat illness because of fever or
dehydration.114–116
History of Heat Illness. Some individuals with a history
of heat illness are at greater risk for recurrent heat illness.8,117
Increased Body Mass Index (Thick Fat Layer or Small
Surface Area). Obese individuals are at an increased risk for
heat illness because the fat layer decreases heat loss.118 Obese
persons are less efficient and have a greater metabolic heat
production during exercise. Conversely, muscle-bound individuals have increased metabolic heat production and a lower
ratio of surface area to mass, contributing to a decreased ability to dissipate heat.119–121
Wet-Bulb Globe Temperature on Previous Day and
Night. When the WBGT is high to extreme (see Table 3), the
risk of heat-related problems is greater the next day; this appears to be one of the best predictors of heat illness.121 Athletes who sleep in cool or air-conditioned quarters are at less
risk.
Poor Physical Condition. Individuals who are untrained
are more susceptible to heat illness than are trained athletes.
As the V̇O2max of an individual improves, the ability to withstand heat stress improves independent of acclimatization and
heat adaptation.122 High-intensity work can easily produce
1000 kcal/h and elevate the core temperature of at-risk individuals (those who are unfit, overweight, or unacclimatized)
to dangerous levels within 20 to 30 minutes.123
Excessive or Dark-Colored Clothing or Equipment. Excessive clothing or equipment decreases the ability to thermoregulate, and dark-colored clothing or equipment may
cause a greater absorption of heat from the environment. Both
should be avoided.113
Overzealousness. Overzealous athletes are at a higher risk
for heat illness because they override the normal behavioral
adaptations to heat and decrease the likelihood of subtle cues
being recognized.
Journal of Athletic Training
335
Lack of Acclimatization to Heat. An athlete with no or
minimal physiologic acclimatization to hot conditions is at an
increased risk of heat-related illness.8,37,83,124
Medications and Drugs. Athletes who take certain medications or drugs, particularly medications with a dehydrating
effect, are at an increased risk for a heat illness.101–106,125–136
Alcohol, caffeine, and theophylline at certain doses are mild
diuretics.106,137,138 Caffeine is found in coffee, tea, soft drinks,
chocolate, and several over-the-counter and prescription medications.139 Theophylline is found mostly in tea and anti-asthma medications.140
Electrolyte Imbalance. Electrolyte imbalances do not usually occur in trained, acclimatized individuals who engage in
physical activity and eat a normal diet.141 Most sodium and
chloride losses in athletes occur through the urine, but athletes
who sweat heavily, are salty sweaters, or are not heat acclimatized can lose significant amounts of sodium during activity.142 Electrolyte imbalances often contribute to heat illness
in older athletes who use diuretics.143,144
Predisposing Medical Conditions
The following predisposing medical conditions add to the
risk of heat illness.
Malignant Hyperthermia. Malignant hyperthermia is
caused by an autosomal dominant trait that causes muscle rigidity, resulting in elevation of body temperature due to the
accelerated metabolic rate in the skeletal muscle.145–147
Neuroleptic Malignant Syndrome. Neuroleptic malignant
syndrome is associated with the use of neuroleptic agents and
antipsychotic drugs and an unexpected idiopathic increase in
core temperature during exercise.148–151
Arteriosclerotic Vascular Disease. Arteriosclerotic vascular disease compromises cardiac output and blood flow
through the vascular system by thickening the arterial
walls.115,152
Scleroderma. Scleroderma is a skin disorder that decreases
sweat production, thereby decreasing heat transfer.149,153
Cystic Fibrosis. Cystic fibrosis causes increased salt loss in
sweat and can increase the risk for hyponatremia.154,155
Sickle Cell Trait. Sickle cell trait limits blood-flow distribution and decreases oxygen-carrying capacity. The condition
is exacerbated by exercise at higher altitudes.156,157
Environmental Risk Factors
When the environmental temperature is above skin temperature, athletes begin to absorb heat from the environment and
depend entirely on evaporation for heat loss.113,158,159 High
relative humidity inhibits heat loss from the body through
evaporation.61
The environmental factors that influence the risk of heat
illness include the ambient air temperature, relative humidity
(amount of water vapor in the air), air motion, and the amount
of radiant heat from the sun or other sources.2,9,41 The relative
risk of heat illness can be calculated using the WBGT equation.2,43,50,69,77,160,161 Using the WBGT index to modify activity in high-risk settings has virtually eliminated heat-stroke
deaths in United States Marine Corps recruits.159 Wet-bulb
globe temperature is calculated using the wet-bulb (wb), drybulb (db), and black-globe (bg) temperature with the following
equation49,62,85,162,163:
WBGT 5 0.7Twb 1 0.2Tbg 1 0.1Tdb
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• Number 3 • September 2002
When there is no radiant heat load, Tdb 5 Tbg, and the equation is reduced62 to
WBGT 5 0.7Twb 1 0.3Tdb
This equation is used to estimate risk as outlined in Table
3.13,40,50,61,85 This index was determined for athletes wearing
a T-shirt and light pants.158 The WBGT calculation can be
performed using information obtained from electronic devices42 or the local meteorologic service, but conversion tables
for relative humidity and Tdb are needed to calculate the wetbulb temperature.50,162 The predictive value from the meteorologic service is not as accurate as site-specific data for representing local heat load but will suffice in most situations.
When WBGT measures are not possible, environmental heat
stress can be estimated using a sling psychrometer (see Figures
1, 2).
Several recommendations have been published for distance
running, but these can also be applied to other continuous
activity sports. The Canadian Track and Field Association recommended that a distance race should be cancelled if the
WBGT is greater than 26.78C (808F).39 The American College
of Sports Medicine guidelines from 1996 recommended that a
race should be delayed or rescheduled when the WBGT is
greater than 27.88C (828F).31,72,73 In some instances, the event
will go on regardless of the WBGT; ATCs should then have
an increased level of suspicion for heat stroke and focus on
hydration, emergency supplies, and detection of exertional
heat illnesses.
Thermoregulation
Thermoregulation is a complex interaction among the central nervous system (CNS), the cardiovascular system, and the
skin to maintain a body-core temperature of 378C.9,43,51,164
The CNS temperature-regulation center is located in the hypothalamus and is the site where the core temperature setpoint
is determined.9,43,82,158,164–166 The hypothalamus receives information regarding body-core and shell temperatures from peripheral skin receptors and the circulating blood; body-core
temperature is regulated through an open-ended feedback loop
similar to that in a home thermostat system.158,165,167,168 Body
responses for heat regulation include cutaneous vasodilation,
increased sweating, increased heart rate, and increased respiratory rate.38,43,51,164,165
Body-core temperature is determined by metabolic heat production and the transfer of body heat to and from the surrounding environment using the following heat-production and
heat-storage equation166,167:
S 5 M 6 R 6 K 6 Cv 2 E
where S is the amount of stored heat, M is the metabolic heat
production, R is the heat gained or lost by radiation, K is the
conductive heat lost or gained, Cv is the convective heat lost
or gained, and E is the evaporative heat lost.
Basal metabolic heat production fasting and at absolute rest
is approximately 60 to 70 kcal/h for an average adult, with
50% of the heat produced by the internal organs. Metabolic
heat produced by intense exercise may approach 1000
kcal/h,51,164 with greater than 90% of the heat resulting from
muscle metabolism.9,40,42,166
Heat is gained or lost from the body by one or more of the
following mechanisms9,85:
Table 4. Physiologic Responses After Heat Acclimatization
Relative to Nonacclimatized State
Physiologic Variable
Heart rate
Stroke volume
Body-core temperature
Skin temperature
Sweat output/rate
Onset of sweat
Evaporation of sweat
Salt in sweat
Work output
Subjective discomfort (rating of
perceived exertion [RPE])
Fatigue
Capacity for work
Mental disturbance
Syncopal response
Extracellular fluid volume
Plasma volume
After Acclimatization
(10–14 Days’ Exposure)
Decreases46,145
Increases145,147
Decreases145
Decreases152
Increases46,47,149
Earlier in training46,145
Increases47,152
Decreases9,50
Increases46,50
Decreases50,145
Decreases50
Increases46,50
Decreases50
Decreases9,50
Increases50
Increases50,150
Radiation. The energy is transferred to or from an object
or body via electromagnetic radiation from higher to lower
energy surfaces.9,43,51,85,166
Conduction. Heat transfers from warmer to cooler objects
through direct physical contact.9,43,51,85,166 Ice packs and coldwater baths are examples of conductive heat exchange.
Convection. Heat transfers to or from the body to surrounding moving fluid (including air).9,43,51,85,166 Moving air from
a fan, cycling, or windy day produces convective heat exchange.
Evaporation. Heat transfers via the vaporization of sweat§
and is the most efficient means of heat loss.51,158,169 The evaporation of sweat from the skin depends on the water saturation
of the air and the velocity of the moving air.170–172 The effectiveness of this evaporation for heat loss from the body diminishes rapidly when the relative humidity is greater than
60%.9,20,164
Cognitive performance and associated CNS functions deteriorate when brain temperature rises. Signs and symptoms
include dizziness, confusion, behavior changes, coordination
difficulties, decreased physical performance, and collapse due
to hyperthermia.168,173 The residual effects of elevated brain
temperature depend on the duration of the hyperthermia. Heat
stroke rarely leads to permanent neurologic deficits51; however, some sporadic symptoms of frontal headache and sleep
disturbances have been noted for up to 4 months.168,174,175
When permanent CNS damage occurs, it is associated with
cerebellar changes, including ataxia, marked dysarthria, and
dysmetria.174
Heat Acclimatization
Heat acclimatization is the physiologic response produced
by repeated exposures to hot environments in which the capacity to withstand heat stress is improved.14,43,75,176,177 Physiologic responses to heat stress are summarized in Table 4.
Exercise heat exposure produces progressive changes in thermoregulation that involve sweating, skin circulation, thermoregulatory setpoint, cardiovascular alterations, and endocrine
§References 9, 40, 43, 50, 51, 85, 159, 165, 166.
adjustments.29,43,178 Individual differences affect the onset and
decay of acclimatization.29,45,179 The rate of acclimatization is
related to aerobic conditioning and fitness; more conditioned
athletes acclimatize more quickly.43,45,180 The acclimatization
process begins with heat exposure and is reasonably protective
after 7 to 14 days, but maximum acclimatization may take 2
to 3 months.45,181,182 Heat acclimatization diminishes by day
6 when heat stress is no longer present.180,183 Fluid replacement improves the induction and effect of heat acclimatization.184–187 Extra salt in the diet during the first few days of
heat exposure also improves acclimatization; this can be accomplished by encouraging the athlete to eat salty foods and
to use the salt shaker liberally during meals.
Cumulative Dehydration
Cumulative dehydration develops insidiously over several
days and is typically observed during the first few days of a
season during practice sessions or in tournament competition.
Cumulative dehydration can be detected by monitoring daily
prepractice and postpractice weights. Even though a small decrease in body weight (less than 1%) may not have a detrimental effect on the individual, the cumulative effect of a 1%
fluid loss per day occurring over several days will create an
increased risk for heat illness and a decrease in performance.110
During intense exercise in the heat, sweat rates can be 1 to
2.5 L/h (about 1 to 2.25 kilograms [2 to 5 pounds] of body
weight per hour) or more, resulting in dehydration. Unfortunately, the volume of fluid that most athletes drink voluntarily
during exercise replaces only about 50% of body-fluid losses.188 Ideally, rehydration involves drinking at a rate sufficient
to replace all of the water lost through sweating and urination.60,77 If the athlete is not able to drink at this rate, he or
she should drink the maximum tolerated. Use caution to ensure
that athletes do not overhydrate and put themselves at risk for
the development of hyponatremia. However, hydration before
an event is essential to help decrease the incidence of heat
illnesses. For more information on this topic, see the ‘‘National
Athletic Trainers’ Association Position Statement: Fluid Replacement in Athletes.’’52
Cooling Therapies
The fastest way to decrease body-core temperature is immersion of the trunk and extremities into a pool or tub filled
with cold water (between 18C [358F] and 158C [598F]).39,88,91,97
Conditions that have been associated with immersion therapy
include shivering and peripheral vasoconstriction; however,
the potential for these should not deter the medical staff from
using immersion therapy for rapid cooling. Shivering can be
prevented if the athlete is removed from the water once rectal
temperature reaches 38.38C to 38.98C (1018F to 1028F). Peripheral vasoconstriction may occur, but the powerful cooling
potential of immersion outweighs any potential concerns. Cardiogenic shock has also been a proposed consequence of immersion therapy, but this connection has not been proven in
cooling heat-stroke patients.39 Cold-water immersion therapy
was associated with a zero percent fatality rate in 252 cases
of exertional heat stroke in the military.89 Other forms of cooling (water spray; ice packs covering the body; ice packs on
axillae, groin, and neck; or blowing air) decrease body-core
temperature at a slower rate compared with cold-water im-
Journal of Athletic Training
337
mersion.97 If immersion cooling is not being used, cooling
with ice bags should be directed to as much of the body as
possible, especially the major vessels in the armpit, groin, and
neck regions (and likely the hands and feet), and cold towels
may be applied to the head and trunk because these areas have
been demonstrated on thermography173,189 to have the most
rapid heat loss.
SPECIAL CONCERNS
Most research related to heat illness has been performed on
normal, healthy adults. Child athletes, older athletes, and athletes with spinal-cord injuries have been studied less frequently. The following are suggestions for special populations or
those with special conditions.
Children (Prepubescents)
Exercise in hot environments and heat tolerance are affected
by many physiologic factors in children. These include decreased sweat gland activity,190 higher skin temperatures,191–193
decreased cardiac output (increased heart rate and lower stroke
volume) due to increased peripheral circulation,194 decreased
exercise economy,195 decreased ability to acclimatize to heat
(slower and takes longer),192 smaller body size (issues related
to body surface-to-mass ratio), maturational differences,190
and predisposing conditions (obesity, hypohydration, childhood illnesses, and other disease states).190,192,196
• Decrease the intensity of activities that last longer than 30
minutes,197 and have the athlete take brief rests50 if the
WBGT is between 22.88C and 27.88C (738F and 828F); cancel or modify the activity if the WBGT is greater than
27.88C (828F).31,69–73 Modification could involve longer and
more frequent rest breaks than are usually permitted within
the rules of the sport (eg, insert a rest break before halftime).
• Encourage children to ingest some fluids at least every 15
to 30 minutes during activity to maintain hydration, even if
they are not thirsty.197
• Use similar precautions as listed earlier for adults.
Older Athletes (.50 Years Old)
The ability of the older athlete to adapt is partly a function
of age and also depends on functional capacity and physiologic
health status.198–206
• The athlete should be evaluated by a physician before exercise, with the potential consequences of predisposing medical conditions and illnesses addressed.9,34–36 An increase
has been shown in the exercise heart rate of 1 beat per minute for each 18C (1.88F) increase in ambient temperature
above neutral (23.98C [758F]).207 Athletes with known or
suspected heart disease should curtail activities at lower temperatures than healthy athletes and should have cardiovascular stress testing before participating in hot environments.
• Older athletes have a decreased ability to maintain an adequate plasma volume and osmolality during exercise,198,208
which may predispose them to dehydration. Regular fluid
intake is critical to avoid hyperthermia.
Athletes with Spinal-Cord Injuries
As sport participation for athletes with spinal-cord injuries
increases from beginner to elite levels, understanding the dis-
338
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• Number 3 • September 2002
ability,209,210 training methods, and causes of heat injury will
help make competition safer.211 For example, the abilities to
regulate heart rate, circulate the blood volume, produce sweat,
and transfer heat to the surface vary with the level and severity
of the spinal-cord lesion.208,212–218
• Monitor these athletes closely for heat-related problems. One
technique for determining hyperthermia is to feel the skin
under the arms of the distressed athlete.211 Rectal temperature may not be as accurate for measuring core temperature
as in other athletes due to decreased ability to regulate blood
flow beneath the spinal-cord lesion.218–220
• If the athlete is hyperthermic, provide more water, lighter
clothing, or cooling of the trunk,211,213 legs,211 and head.213
HOSPITALIZATION AND RECOVERY
After an episode of heat stroke, the athlete may experience
impaired thermoregulation, persistent CNS dysfunction,221,222
hepatic insufficiency, and renal insufficiency.39,223 For persons
with exertional heat stroke and associated multisystem tissue
damage, the rate of recovery is highly individualized, ranging
up to more than 1 year.8,86,221 In one study, 9 of 10 patients
exhibited normal heat-acclimatization responses, thermoregulation, whole-body sodium and potassium balance, sweatgland function, and blood values about 2 months after the heat
stroke.8 Transient or persistent heat intolerance was found in
a small percentage of patients.83 For some athletes, a history
of exertional heat stroke increases the chance of experiencing
subsequent episodes.39
An athlete who experiences heat stroke may have compromised heat tolerance and heat acclimatization after physician
clearance.35,224,225 Decreased heat tolerance may affect 15%
to 20% of persons after a heat stroke-related collapse,226,227
and in a few individuals, decreased heat tolerance has persisted
up to 5 years.35,224,228 Additional heat stress may reduce the
athlete’s ability to train and compete due to impaired cardiovascular and thermoregulatory responses.115,228–230
After recovery from an episode of heat stroke or hyponatremia, an athlete’s physical activity should be restricted8,86
and the gradual return to sport individualized by his or her
physician. The athlete should be monitored on a daily basis
by the ATC during exercise.86 During the return-to-exercise
phase, an athlete may experience some detraining and deconditioning not directly related to the heat exposure.8,86 Evaluate
the athlete over time to determine whether there has been a
complete recovery of exercise and heat tolerance.8,86
CONCLUSIONS
Athletic trainers and other allied health providers must be
able to differentiate exercise-associated muscle (heat) cramps,
heat syncope, exercise (heat) exhaustion, exertional heat
stroke, and exertional hyponatremia in athletes.
This position statement outlines the NATA’s current recommendations to reduce the incidence, improve the recognition, and optimize treatment of heat illness in athletes. Education and increased awareness will help to reduce both the
frequency and the severity of heat illness in athletes.
ACKNOWLEDGMENTS
This pronouncement was reviewed for the NATA by the Pronouncements Committee, Edward R. Eichner, MD, FACSM, and Wil-
liam O. Roberts, MD, MS, FACSM. T. Kyle Eubanks, MA, ATC,
and Paul C. Miller, PhD, provided assistance in the preparation of
the manuscript.
26.
27.
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Journal of Athletic Training
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Journal of Athletic Training
2008;43(6):640–658
g by the National Athletic Trainers’ Association, Inc.
www.nata.org/jat
position statement
National Athletic Trainers’ Association Position
Statement: Environmental Cold Injuries
Thomas A. Cappaert, PhD, ATC, CSCS, CES*; Jennifer A. Stone, MS, ATC,
CSCS; John W. Castellani, PhD, FACSM`; Bentley Andrew Krause, PhD,
ATC‰; Daniel Smith, ATC, CSTS, ARTI; Bradford A. Stephens, MD, PC"
*Central Michigan University, Mt Pleasant, MI; 3Monument, CO; 4US Army Research Institute of Environmental
Medicine, Natick, MA; 1Ohio University, Athens, OH; IUnited States Luge Association, Lake Placid, NY; "Lake Placid
Sports Medicine, Lake Placid, NY
Objective: To present recommendations for the prevention,
recognition, and treatment of environmental cold injuries.
Background: Individuals engaged in sport-related or workrelated physical activity in cold, wet, or windy conditions are at
risk for environmental cold injuries. An understanding of the
physiology and pathophysiology, risk management, recognition,
and immediate care of environmental cold injuries is an
essential skill for certified athletic trainers and other health care
providers working with individuals at risk.
Recommendations: These recommendations are intended
to provide certified athletic trainers and others participating
in athletic health care with the specific knowledge and
problem-solving skills needed to address environmental cold
injuries. Each recommendation has been graded (A, B, or C)
according to the Strength of Recommendation Taxonomy
criterion scale.
Key Words: environmental physiology, hypothermia, frostbite, frostnip, chilblain, pernio, immersion foot, trench foot
C
PURPOSES
old injuries are a common result of exposure to cold
environments during physical activity or occupational pursuits. Many individuals engage in fitness
pursuits and physical activity year-round in environments
with cold, wet, or windy conditions (or a combination of
these), thereby placing themselves at risk of cold injuries.
The occurrence of these injuries depends on the combination of 2 factors: low air or water temperatures (or both)
and the influence of wind on the body’s ability to maintain
a normothermic core temperature, due to localized
exposure of the extremities to cold air or surfaces. Cold
injuries and illnesses occur in a wide range of physically
active individuals, including military personnel, traditional
winter-sport athletes, and outdoor-sport athletes, such as
those involved in running, cycling, mountaineering, and
swimming. Traditional team sports such as football,
baseball, softball, soccer, lacrosse, and track and field
have seasons that extend into late fall or early winter or
begin in early spring, when weather conditions can increase
susceptibility to cold injury. Reported rates of hypothermia
and frostbite include 3% to 5% of all injuries in
mountaineers and 20% of all injuries in Nordic skiers.1
Cold injury frequency in military personnel is reported to
range from 0.2 to 366 per 1000 exposures.1–6
As the scope of physical activity participation broadens
(eg, extreme sports, adventure racing) and environments
with the potential for extreme weather conditions become
more accessible, a review of cold injury physiology,
prevention, recognition, treatment, and management is
warranted. Clinicians practicing in settings or geographic
regions that predispose individuals to cold injury must be
aware of these risks and implement strategies to prevent
cold injuries and to minimize them when they occur.
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This position statement includes a review of available
literature, definitions of cold injuries, and a set of
recommendations that will allow certified athletic trainers
(ATs) and other allied health and medical providers to
1.
2.
3.
4.
5.
Identify and employ prevention strategies to reduce
cold-related injuries and illnesses in the physically
active.
Describe factors associated with cold-related injuries
and illnesses.
Provide on-site first aid and immediate care of coldrelated injuries and illnesses.
Understand the thermoregulatory and physiologic
responses to cold.
Identify groups with unique concerns related to cold
exposure.
DEFINITIONS OF COLD INJURIES
Cold injuries are classified into 3 categories: decreased
core temperature (hypothermia), freezing injuries of the
extremities, and nonfreezing injuries of the extremities.
Each scenario and its characteristic condition(s) will be
described. A summary of the signs and symptoms of these
injuries and illnesses is found in Table 1, with images of the
skin conditions displayed in Figures 1 through 3.
Hypothermia
Traditionally, hypothermia is defined as a decrease in
core body temperature below 956F (356C). Hypothermia is
Table 1. Signs and Symptoms of Cold-Related Injuries
Condition
Hypothermia1,5,7–9
Mild
Core temperature 98.66F to 956F (376C–356C)
Amnesia, lethargy
Vigorous shivering
Impaired fine motor control
Cold extremities
Polyuria
Pallor
Rhinorrhea
Typically conscious
Blood pressure within normal limits
Moderate
Core temperature 946F to 906F (346C–326C)
Depressed respiration and pulse
Cardiac arrhythmias
Cyanosis
Cessation of shivering
Impaired mental function
Slurred speech
Impaired gross motor control
Loss of consciousness
Muscle rigidity
Dilated pupils
Blood pressure decreased or difficult to measure
Severe
Core temperature below 906F (326C)
Rigidity
Bradycardia
Severely depressed respiration
Hypotension, pulmonary edema
Spontaneous ventricular fibrillation or cardiac arrest
Usually comatose
Frostbite1,5,8–13
Mild/superficial
Deep
Chilblain/pernio5,13,14
Immersion (trench) foot5,8,14
a
Sign or Symptoma
Dry, waxy skin
Erythema
Edema
Transient tingling or burning sensation
Skin contains white or blue-gray colored patches
Affected area feels cold and firm to the touch
Limited movement of affected area
Skin is hard and cold
Skin may be waxy and immobile
Skin color is white, gray, black, or purple
Vesicles present
Burning aching, throbbing, or shooting pain
Poor circulation in affected area
Progressive tissue necrosis
Neurapraxia
Hemorrhagic blistering develops within 36 to 72 hours
Muscle, peripheral nerve, and joint damage likely
Red or cyanotic lesions
Swelling
Increased temperature
Tenderness
Itching, numbness, burning, or tingling
Skin necrosis
Skin sloughing
Burning, tingling, or itching
Loss of sensation
Cyanotic or blotchy skin
Swelling
Pain/sensitivity
Blisters
Skin fissures or maceration
Not all patients will display all signs and symptoms of the condition.
Journal of Athletic Training
641
Figure 1. Frostbite.
Figure 3. Immersion (trench) foot.
classified as mild, moderate, or severe, depending upon
measured core temperature. Information in the literature
varies slightly as to which core temperatures are assigned to
which degree of hypothermia, but in this paper, we will use
the following definitions. Mild hypothermia is a core
temperature of 956F (356C) to 98.66F (376C). Moderate
hypothermia is a core temperature of 906F (326C) to 946F
(346C). Severe hypothermia is a core temperature below
906F (326C).1,7–9 Each level of hypothermia has characteristic signs and symptoms, although individuals respond
differently, and not every hypothermic person exhibits all
signs and symptoms. Therefore, a detailed assessment is
appropriate in all cases of potential cold injury. Hypothermia is most likely to occur with prolonged exposure to
cold, wet, or windy conditions (or a combination of these)
experienced during endurance events, outdoor team sports
(eg, soccer, football), mountaineering, hiking, and military
maneuvers and in occupations that require long periods
outdoors or in unheated spaces (eg, public safety, building
trades, transportation).
Frostbite and Frostnip
Frostbite is actual freezing of body tissues. It is a
localized response to a cold, dry environment, yet moisture
from sweating may exacerbate frostbite due to increased
tissue cooling. Similar to hypothermia, frostbite has stages,
delineated by the depth of tissue freezing and resulting in
frostnip, mild frostbite, or severe frostbite.1,8–13 Frostbite
develops as a function of the body’s protective mechanisms
to maintain core temperature. Warm blood is shunted from
cold peripheral tissues to the core by vasoconstriction of
arterioles, which supply capillary beds and venules to the
extremities and face, especially the nose and ears. Frostbite
progresses from distal to proximal and from superficial to
deep. As the temperature of these areas continues to
decrease, cells begin to freeze. Damage to the frostbitten
tissue is due to electrolyte concentration changes within the
cells, resulting in water crystallization within the tissue. For
cells to freeze, the tissue temperature must be below 286F
(226C).8–13
Frostnip, the mildest form of cold injury to the skin, is a
precursor to frostbite. It can occur with exposure of the
skin to very cold temperatures, often in combination with
windy conditions. It can also occur from skin contact with
cold surfaces (eg, metal, equipment, liquid). With frostnip,
only the superficial skin is frozen; the tissues are not
permanently damaged, although they may be more
sensitive to cold and more likely, with repeated exposures,
to develop frostnip or frostbite.8–13 Mild frostbite involves
freezing of the skin and adjacent subcutaneous tissues;
extracellular water freezes first, followed by cell freezing.
Severe frostbite is freezing of the tissues below the skin and
the adjacent tissues, which can include muscle, tendon, and
bone.8–13
Chilblain (Pernio)
Figure 2. Chilblain. Photograph reprinted with permission:
gChristoph U. Lehmann, MD, Dermatlas; http://www.dermatlas.org.
642
Volume 43
N Number 6 N December 2008
Chilblain, also known as pernio, is an injury associated
with extended exposure (1–5 hours) to cold, wet conditions. Chilblain is an exaggerated or uncharacteristic
inflammatory response to cold exposure. Prolonged
constriction of the skin blood vessels results in hypoxemia
and vessel wall inflammation; edema in the dermis may
also be present. Chilblain can occur with or without
a
Table 2. Strength of Recommendation Taxonomy (SORT)
Strength of Recommendation
Definition
A
Recommendation based upon consistent and good quality patient-oriented evidence (morbidity, mortality,
symptom improvement, cost reduction, and quality of life).
Recommendation based on inconsistent or limited-quality patient-oriented evidence.
Recommendation based on consensus, usual practice, opinion, disease-oriented evidence (measures of
intermediate, physiologic, or surrogate end-points that may or may not reflect improvements in patient
outcomes), or case series for studies of diagnosis, treatment, prevention, or screening.
B
C
a
Adapted or reprinted with permission from ‘Strength of Recommendation Taxonomy (SORT) A Patient Centered Approach to Grading Evidence in
the Medical Literature,’ February 12004, American Family Physician. Copyright g2004 American Academy of Family Physicians. All Rights
Reserved.
freezing of the tissue. The hands and feet are most
commonly affected, but chilblain of the thighs has also
been reported.14 Situations in which this can happen
include alpine sports, mountaineering, hiking, endurance
sports, and team sports in which footwear and clothing
remain wet for prolonged periods due to water exposure or
sweating.
Chilblain severity is time and temperature related. The
higher the temperature of the water (generally ranging
from 326F [06C] to 606F [166C]), the longer the duration of
exposure required to develop chilblain. Time of exposure is
usually measured in hours or even days, rather than the
minutes or hours associated with frostbite. Chilblain and
immersion foot (see below) occur in similar environments,
but the former is a more superficial injury and can develop
in a shorter time period than the latter.13,14
Immersion (Trench) Foot. Immersion foot typically
occurs with prolonged exposure (12 hours to 4 days) to
cold, wet conditions, usually in temperatures ranging from
326F to 656F (06C–186C). This condition affects primarily
the soft tissues, including nerves and blood vessels, due to
an inflammatory response that results in high levels of
extracellular fluid. The most common mechanism for
developing immersion foot is the continued wearing of
wet socks or footwear (or both).8,14
complete elimination of cold-related injuries but may
decrease risk. The National Athletic Trainers’ Association
(NATA) promotes the following approaches for prevention,
recognition, and treatment of cold-related injuries.
EVIDENCE CLASSIFICATION
4.
In this position statement, we present recommendations
using an evidence-based review and the Strength of
Recommendation Taxonomy (SORT) criterion scale (Table 2) proposed by the American Academy of Family
Physicians.15 The recommendations are given a grade of A,
B, or C based upon evidence using patient or diseaseoriented outcomes (treatments or practices). Little outcomes-based research using randomized clinical trials on
cold injury has been performed due to ethical constraints
regarding standards of care and difficulties procuring large
sample groups. These limitations should be weighed when
assessing specific recommendations.
Prevention
1.
2.
3.
5.
RECOMMENDATIONS
Recommendations are presented to help ATs and other
health care providers minimize risks to the health and safety
of physically active individuals exposed to cold environments
and provide effective immediate care when needed. Individual responses to cold vary physiologically with combinations
of cold, wet, and windy conditions as well as clothing
insulation, exposure time, and other nonenvironmental
factors. Therefore, these recommendations do not guarantee
6.
Perform a comprehensive, physician-supervised, preparticipation medical screening to identify athletes
with a previous history of cold injury and athletes
predisposed to cold injury based upon known risk
factors (Table 3). This preparticipation examination
should include questions pertaining to a history of
cold injury and problems with cold exposure16 and
should be performed before planned exposures to
conditions that may lead to cold injury. Evidence
Category: C
Identify participants who present with known risk
factors (Table 3) for cold injury and provide increased
monitoring of these individuals for signs and symptoms.5 Evidence Category: C
Ensure that appropriately trained personnel are
available on-site at the event and are familiar with
cold injury prevention, recognition, and treatment
approaches.5 Evidence Category: C
Educate athletes and coaches concerning the prevention, recognition, and treatment of cold injury and the
risks associated with activity in cold environments.5
Evidence Category: C
Educate and encourage athletes to maintain proper
hydration and eat a well-balanced diet. These guidelines are especially imperative for activities exceeding
2 hours.17–19 Consistent fluid intake during lowintensity exercise is necessary to maintain hydration
in the presence of typical cold-induced diuresis.20–22
Athletes should be encouraged to hydrate even if they
are not thirsty, as evidence suggests the normal thirst
mechanism is blunted with cold exposure.23 Evidence
Category: C
Develop event and practice guidelines that include
recommendations for managing athletes participating
in cold, windy, and wet conditions.24,25 The influence
of air temperature and wind speed conditions should
be taken into account by using wind-chill guidelines.26,27 Risk management guidelines (Table 3, Figure 4) can be used to make participation decisions
based upon the prevailing conditions. Participation
Journal of Athletic Training
643
decisions depend upon the length of anticipated
exposure and availability of facilities and interventions
for rewarming if needed. Modify activity in high-risk
conditions to prevent cold injury. Monitor athletes for
signs and symptoms and be prepared to intervene with
basic treatment. Also monitor environmental conditions before and during the activity and adjust
activities if weather conditions change or degenerate.28,29 Evidence Category: C
7. Clothing should provide an internal layer that allows
evaporation of sweat with minimal absorption, a
middle layer that provides insulation, and a removable
external layer that is wind and water resistant and
allows for evaporation of moisture. Examples of
various clothing ensembles are found in Table 4.
Toes, fingers, ears, and skin should be protected when
wind-chill temperatures are in the range at which
frostbite is possible in 30 minutes or less. Remove wet
clothing as soon as practical and replace with dry,
clean items.30–32 Evidence Category: C
8. Provide the opportunity for athletes to rewarm, as
needed, during and after activity using external
heaters, a warm indoor environment, or the addition
of clothing. After water immersion, rewarming
should begin quickly and the athlete should be
monitored for afterdrop, in which the core temperature actually decreases during rewarming. 33–35
Evidence Category: C
9. Include the following supplies on the field, in the
locker room, or at convenient aid stations for
rewarming purposes:
N A supply of water or sports drinks for rehydration
purposes as well as warm fluids for possible
rewarming purposes. Fluids that may freeze during
events in subfreezing temperatures may need to be
placed in insulated containers or replaced intermittently.
N Heat packs, blankets, additional clothing, and
external heaters, if feasible, for active rewarming.
N Flexible rectal thermometer probe to assess core
body temperature. Rectal temperature has been
identified as the best combination of practicality
and accuracy for assessing core temperature in the
field.36 Other measurements (tympanic, aural, and
esophageal) are problematic or difficult to obtain.
The rectal thermometer used should be a lowreading thermometer (ie, capable of measuring
temperatures below 956F [356C]).
N Telephone or 2-way radio to communicate with
additional medical personnel and to summon emergency medical transportation.
N Tub, wading pool, or whirlpool for immersion
warming treatments (including a thermometer and
additional warm water to maintain required temperatures). Evidence Category: C
10. Notify area hospital and emergency personnel before
large events to inform them of the potential for coldrelated injuries. Evidence Category: C
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Recognition and Treatment
Hypothermia (Mild)
11. Be aware of the signs and symptoms of hypothermia,
which include vigorous shivering, increased blood
pressure, rectal temperature less than 98.66F (376C)
but greater than 956F (356C), fine motor skill
impairment, lethargy, apathy, and mild amnesia
(Table 1). Evidence Category: A
12. Rectal temperature obtained using a thermometer
(digital or mercury) that can read below 946F (346C)
is the preferred method for assessing core temperature in persons suspected of being hypothermic,
even though procuring rectal temperature in the field
can be a challenge. Using tympanic, axillary, or
oral temperatures instead of rectal temperature is
faulty due to environmental concerns, such as
exposure to air temperatures; however, if either
axillary or oral temperature is above 956F (356C),
the person is not hypothermic.1,7–9 Figure 5 provides
a treatment algorithm for hypothermia. Evidence
Category: B
13. Begin by removing wet or damp clothing; insulating
the athlete with warm, dry clothing or blankets
(including covering the head); and moving the athlete
to a warm environment with shelter from the wind and
rain. Evidence Category: C
14. When rewarming, apply heat only to the trunk and
other areas of heat transfer, including the axilla, chest
wall, and groin.37–39 Rewarming the extremities can
produce afterdrop, which is caused by dilation of
peripheral vessels in the arms and legs when warmed.
This dilation sends cold blood, often with a high level
of acidity and metabolic byproducts, from the
periphery to the core. This blood cools the core,
leading to a drop in core temperature, and may result
in cardiac arrhythmias and death. 40,41 Evidence
Category: C
15. Provide warm, nonalcoholic fluids and foods containing 6% to 8% carbohydrates to help sustain shivering
and maintain metabolic heat production. Evidence
Category: C
16. Avoid applying friction massage to tissues, as this may
increase damage if frostbite is present.10 Evidence
Category: A
Hypothermia (Moderate/Severe)
17. Be aware of the signs and symptoms of moderate and
severe hypothermia, which may include cessation of
shivering, very cold skin upon palpation, depressed
vital signs, rectal temperature between 906F (326C)
and 956F (356C) for moderate hypothermia or below
906F (326C) for severe hypothermia, impaired mental
function, slurred speech, unconsciousness, and gross
motor skill impairment (Table 1).1,7–9 Evidence Category: A
18. If an athlete with suspected hypothermia presents with
signs of cardiac arrhythmia, he or she should be
Table 3. Prevention and Risk Management Process for the Certified Athletic Trainer
1. Before event
N Encourage proper hydration and nutrition, and discourage alcohol and drug use.
N Ensure that athletes and coaches know the signs and symptoms of cold injury.
N Identify participants at a high risk of cold injury. Risk factors include the following:
#
Lean body composition
#
Females
#
Older age
#
Black race
#
Lower fitness level
#
Presence of comorbidity (eg, cardiac disease, anorexia, Raynaud syndrome, exercise-induced bronchospasm)
N Encourage proper conditioning and appropriate equipment and clothing choices.
2. Environmental assessment
N
N
N
N
Evaluate immediate and projected weather information, including air temperature, wind, chance of precipitation or water immersion, and altitude.
Identify activity intensity requirements and clothing requirements for each individual.
Have alternate plans in place for deteriorating conditions and activities that must be adjusted or cancelled.
The following guidelines can be used in planning activity depending on the wind-chill temperature. Conditions should be constantly reevaluated
for change in risk, including the presence of precipitation:
#
306F (21.116C) and below: Be aware of the potential for cold injury and notify appropriate personnel of the potential.
#
256F (23.896C) and below: Provide additional protective clothing, cover as much exposed skin as practical, and provide opportunities and
facilities for rewarming.
#
156F (29.446C) and below: Consider modifying activity to limit exposure or to allow more frequent chances to rewarm.
#
06F (217.786C) and below: Consider terminating or rescheduling activity.
3. Coaches’ and athletes’ roles
N Coordinate a schedule of hydration and/or feeding.
N Coordinate a schedule of rewarming or clothing changes as needed.
N Identify possible activity modifications as conditions change (eg, change activity times, allow more frequent chances to rewarm, allow changes
to clothing or equipment).
N Become educated about the prevention and recognition of cold injuries.
N Develop a schedule for monitoring athletes to allow early recognition of potential injury.
4. Event management
N
N
N
N
N
Provide food and fluids.
Provide warming facilities.
Provide additional clothing and equipment for varying conditions.
Implement exposure control and rewarming schedules as needed.
Monitor environmental conditions and athletes regularly.
5. Treatment preparations
N
N
N
N
N
N
Ensure medical staff is prepared to identify the signs and symptoms of cold injury.
Ensure medical staff has proper equipment and skills to assess cold injury, including assessment of low core temperatures.
Prepare an emergency action plan in the event that rapid transport is necessary.
Prepare active rewarming equipment (eg, whirlpool, hot packs, towels, blankets, dry clothing).
Identify warm, dry areas for athletes to passively rewarm, recover, or receive treatment.
Provide direct on-site (ie, sideline) means of passive rewarming (eg, additional clothing, space heaters).
moved very gently to avoid causing paroxysmal
ventricular fibrillation.7–9 Evidence Category: B
19. Begin with a primary survey to determine the necessity
of cardiopulmonary resuscitation (CPR) and activation of the emergency medical system. Remove wet or
damp clothing; insulate the athlete with warm, dry
clothing or blankets (including covering the head); and
move the athlete to a warm environment with shelter
from the wind and rain. Evidence Category: C
20. When rewarming, apply heat only to the trunk and
other areas of heat transfer, including the axilla, chest
wall, and groin.37–39 Evidence Category: C
21. If a physician is not present during the treatment
phase, initiate rewarming strategies immediately and
continue rewarming during transport and at the
hospital. Evidence Category: C
22. During the treatment and/or transport, continually
monitor vital signs and be prepared for airway
management. A physician may order more aggressive
rewarming procedures, including inhalation rewarming, heated intravenous fluids, peritoneal lavage,
blood rewarming, and use of antiarrhythmia
drugs.41–46 Evidence Category: C
23. When immediate management is complete, monitor
for postrewarming complications, including infection
and renal failure.47 Evidence Category: A
Frostbite (Superficial)
24. Be aware of signs and symptoms of superficial
frostbite, which include edema, redness or mottled
gray skin appearance, stiffness, and transient tingling
or burning (Table 1, Figure 1). Evidence Category: A
Journal of Athletic Training
645
25. Rule out the presence of hypothermia by evaluating
observable signs and symptoms and measuring core
temperature. Evidence Category: C
26. The decision to rewarm an athlete is contingent upon
resources available and likelihood of refreezing.
Rewarming can occur at room temperature or
by placing the affected tissue against another
person’s warm skin. Rewarming should be performed slowly, and water temperatures greater than
986F to 1046F (376C–406C) should be avoided.
Evidence Category: C
27. If rewarming is not undertaken, protect the affected
area from additional damage and further tissue
temperature decreases and consult with a physician
or transport to a medical facility.48–50 Evidence
Category: C
28. Avoid applying friction massage to tissues and leave
any vesicles (fluid-filled blisters) intact.48–50 Evidence
Category: C
29. Once rewarming has begun, it is imperative that
affected tissue not be allowed to refreeze, as tissue
necrosis usually results.48–50 Evidence Category: C
30. Athletes should avoid consuming alcohol and using
nicotine.5 Evidence Category: B
Frostbite (Deep)
31. Be aware of signs and symptoms of deep frostbite,
which include edema, mottled or gray skin appearance, tissue that feels hard and does not rebound,
vesicles, and numbness or anesthesia (Table 1).10–12
Evidence Category: A
32. Rule out the presence of hypothermia by assessing
observable signs and symptoms and measuring core
temperature.10–12,48–50 Evidence Category: C
33. To rewarm, the affected tissue should be immersed in
a warm (986F–1046F [376C–406C]) water bath. Water
temperature should be monitored and maintained.
Remove any constrictive clothing and submerge the
entire affected area. The water will need to be gently
circulated, and the area should be immersed for 15 to
30 minutes. Thawing is complete when the tissue is
pliable and color and sensation have returned.
Rewarming can result in significant pain, so a
physician may prescribe appropriate analgesic medication. Evidence Category: C
34. If rewarming is not undertaken, the affected area
should be protected from additional damage and
further tissue temperature decreases. Consult with a
physician or transport the athlete to a medical
facility.48–50 Evidence Category: C
35. Tissue plasminogen activators (tPA) may be administered to improve tissue perfusion. These agents
have been shown to limit the need for subsequent amputation due to tissue death.51 Evidence
Category: B
36. Do not use dry heat or steam to rewarm affected
tissue.48–50 Evidence Category: C
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N Number 6 N December 2008
37. Avoid friction massage or vigorous rubbing to the
affected tissues and leave any vesicles or fluid-filled
blisters intact. If vesicles rupture, they should be
treated to prevent infection.48–50 Evidence Category: C
38. Once rewarming has begun, it is imperative that the
affected tissue not be allowed to refreeze, as tissue
necrosis usually results. Also, weight bearing should
be avoided when feet are affected. If the possibility of
refreezing exists, rewarming should be delayed until
advanced medical care can be obtained.48–50 Evidence
Category: C
39. Athletes should avoid using alcohol and nicotine.48–50
Evidence Category: B
40. If tissue necrosis occurs and tissue sloughs off,
debridement and infection control measures are
appropriate.48–50 Evidence Category: B
Chilblain
41. Be aware of the signs and symptoms of chilblain,
which include exposure to cold, wet conditions for
more than 60 minutes at temperatures less than 506F
(166C) and the presence of small erythematous
papules, with edema, tenderness, itching, and pain
(Table 1, Figure 2). Upon rewarming, the skin may
exhibit inflammation, redness, swelling, itching, or
burning and increased temperature.14 Evidence Category: A
42. Remove wet or constrictive clothing, wash and dry
the area gently, elevate the area, and cover with
warm, loose, dry clothing or blankets.14 Evidence
Category: C
43. Do not disturb blisters, apply friction massage, apply
creams or lotions, use high levels of heat, or allow
weight bearing on the affected area.14 Evidence
Category: C
44. During treatment, continually monitor the affected
area for return of circulation and sensation.14 Evidence
Category: C
Immersion (Trench) Foot
45. Be aware of the signs and symptoms of immersion
(trench) foot, which include exposure to cold, wet
environments for 12 hours to 3 or 4 days, burning,
tingling or itching, loss of sensation, cyanotic or
blotchy skin, swelling, pain or sensitivity, blisters, and
skin fissures or maceration (Table 1, Figure 3).8,14
Evidence Category: A
46. To prevent immersion foot, encourage athletes to
maintain a dry environment within the footwear,
which includes frequent changes of socks or footwear
(or both), the use of moisture-wicking sock material,
controlling excessive foot perspiration, and allowing
the feet to dry if wearing footwear that does not allow
moisture evaporation (eg, vinyl, rubber, vapor-barrier
shoes or boots).5,8,14 Evidence Category: C
47. For treatment, thoroughly clean and dry the feet, and
then treat the affected area by applying warm packs or
soaking in warm water (1026F–1106F [396C–436C])
Figure 4. A, United States National Weather Service Wind Chill Chart (figure reproduced from http://www.weather.gov/os/windchill/images/
windchillchart3.pdf). B, Meteorological Society of Canada/EnvironmentCanada Wind-Chill Calculation Chart (figure adapted from http://www.
msc.ec.gc.ca/education/windchill/windchill_chart_e.cfm). Tair = Actual air temperature in 6C; V10 = wind speed at 10 m in km/h (as reported in
weather observations). Temperatures to the left of the bold line are a low risk of frostbite for most people. Increasing indicates within 30 min,
increasing risk of frostbite for most people within 30 minutes of exposure; High, 5 to 10 min, high risk for most people in 5 to 10 minutes of
exposure; High, 2 to 5 min, high risk for most people in 2 to 5 minutes of exposure; and High, #2 min, high risk for most people in #2 minutes
of exposure. Conversions: 6F = (6C 3 9/5) + 32; mile = km 3 0.6214.
for approximately 5 minutes. Replace wet socks with a
clean, dry pair, and rotate footwear or allow footwear
to dry before reusing.8,14 Evidence Category: C
48. Use a risk management process that includes strategies
for preventing, recognizing, and treating cold injuries
during events. These strategies can then be used for
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647
96
Table 4. Approximate Clothing Insulation of Various Clothing Combinations for Cold Weather Exposure
Clothing Combination
Clothing Insulation Factor (clo)
Shirt, lightweight trousers, socks, shoes, underwear briefs
Shirt, trousers, jacket, socks, shoes, underwear briefs
Wind-proof, waterproof jogging suit (jacket and pants), T-shirt, briefs, running shorts, athletic
socks, athletic shoes
Fleece long-sleeved shirt, fleece pants, briefs, athletic socks, athletic shoes
Lightweight jacket, thermal long underwear top and bottoms, briefs, shell pants, athletic
socks, athletic shoes
Lightweight jacket, long-sleeved fleece shirt, fleece pants, briefs, shell pants, athletic socks,
athletic shoes
Ski jacket with detachable fiberfill liner, thermal long underwear bottoms, knit turtleneck,
sweater, fiberfill ski pants, knit hat, goggles, mitten shell with fleece glove inserts, thin
knee-length ski socks, insulated waterproof boots
Extreme cold-weather down-filled parka with hood, shell pants, fiberfill pants liner, thermal
long underwear top and bottoms, sweat shirt, mitten shell with inner fleece gloves, thick
socks, insulated waterproof boots
Extreme cold-weather expedition suit with hood (down-filled, 1 piece), thermal long
underwear top and bottoms, sweat shirt, mitten with fleece liners, thick socks, insulated
waterproof boots
0.6
1
1.03
1.19
1.24
1.67
2.3
3.28
3.67
ISO. This material is reproduced from ISO 9920:2007 with permission of the American National Standards Institute (ANSI) on behalf of the
International Organization for Standardization (ISO). No part of this material may be copied or reproduced in any form, electronic retrieval system or
otherwise or made available on the Internet, a public network, by satellite or otherwise without the prior written consent of the ANSI. Copies of this
standard may be purchased from the ANSI, 25 West 43rd Street, New York, NY 10036, (212) 642-4900, http://webstore.ansi.org.
g
preparing and devising risk management protocols
and plans when cold injuries may be a possibility. An
example of a risk management process is found in
Table 3. Evidence Category: C
BACKGROUND AND LITERATURE REVIEW
Thermoregulation
During cold stress, a normal body temperature is
maintained through a complex regulatory system. A
summary of the interactions among various physiologic
influences and controls is found in Figure 6. Maintaining a
normothermic body temperature depends on a dynamic
balance between heat gained from metabolic heat production and heat lost to the environment.52–58 The body’s basic
responses to cold stress in order to maintain normothermia
are an increase in metabolic heat production, or thermogenesis, and peripheral vasoconstriction at the skin surface
to prevent heat loss to the environment.
An increase in metabolic heat production can be
accomplished in 2 ways: nonshivering thermogenesis and
shivering thermogenesis. Nonshivering thermogenesis is
defined as an increase in metabolic heat production from
sources other than muscle contraction and is not considered a major source of metabolic heat in adult humans.52–58
Shivering thermogenesis is defined as an increase in heat
production due to involuntary muscle contraction.52–60 The
onset and intensity of shivering are mitigated by the
duration and intensity of the cold exposure. The large
muscle groups of the trunk are typically the first muscles to
begin contracting, and the contractions then spread to the
extremities.60 These alterations in body metabolism are
mediated by the efferent output leaving the thermoregulatory center of the hypothalamus. This efferent output is
determined by the integration of afferent input from the
skin and the deep body receptors at the great vessels and by
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the local temperature of the hypothalamic thermoregulatory center itself.58,61
A decrease in peripheral blood flow due to blood vessel
constriction prevents loss of heat to the environment by
reducing the thermal gradient (ie, the temperature difference
between the skin and the environment). The reduction in
peripheral blood flow is highly specific and most pronounced
in the extremities. Neural control of peripheral blood flow is
under the influence of skin temperature, core temperature,
and baroreflexes.53–57,61 The vasoconstriction response
typically begins at a skin temperature of less than 93.26F
to 95.06F (346C–356C)62 and is maximized at skin temperatures of 87.86F (316C) and below.63 The magnitude and
duration of the vasoconstriction is modulated by a coldinduced vasodilation (CIVD). The CIVD appears to limit the
duration of the vasoconstriction and protect the affected area
from local cold injury. Periodic fluctuations in blood flow
create fluctuations in skin temperature after the initial drop
in skin blood flow and temperature with cold exposure. This
fluctuation between minimal and greater-than-normal flow
continues throughout the cold exposure. The CIVD appears
to be mediated by the cessation of norepinephrine release
after initial release. It may also occur due to decreases in
tissue temperature, which diminish sympathetic nerve
conduction and stop the release of norepinephrine. The
resulting blood flow increase rewarms the tissue, nerve
activity is reestablished, norepinephrine is released, and
vasoconstriction is reinitiated. When the CIVD is absent
(which can result from certain drugs; see ‘‘Nonenvironmental
Risk Factors’’) and fails to provide protection, the risk of
nonfreezing cold injury may increase.14,64
Heat Loss Mechanisms
The human body loses heat to the environment through
4 mechanisms: radiation, convection, conduction, and
evaporation. By manipulating environment or clothing
(microenvironment) or both, humans can minimize heat
Figure 5. Algorithm for patient with hypothermia.
Journal of Athletic Training
649
Figure 6. Physiologic responses to cold exposure.
losses. However, with inappropriate choices or when
proper choices are unavailable, heat losses are exacerbated,
with potentially fatal consequences.
Radiation is heat lost directly to the environment by
long-wave (infrared) radiation. Wind, wetness, and other
factors do not affect it. Radiative heat loss is greatest at
night, especially with the absence of the moon or cloud
cover. Uncovered surfaces of the body, especially the head,
face, neck, and hands, also increase radiative heat loss.
Heat lost through uncovered skin is perceived to be greater
because skin temperature is lower and can account for 50%
to 65% of all heat losses from the human body in a resting
state.52
Convection is heat lost through the movement of air or
water across the skin. The human body maintains a thin
layer of warm air adjacent to the skin, called the boundary
layer. Convection enhances the rate of evaporative heat
loss. Air moving across the skin removes this warm layer,
replacing it with a cold layer of air that must then be
warmed. Air movement may be from wind or a person
moving through the air, as in running, skiing, cycling, etc.
Depending upon the speed of the air moving across the
skin, convective heat losses may be small or large. An
estimate of convective heat loss is the wind-chill factor. The
amount and insulative properties of clothing worn may
reduce or intensify convective heat losses.52
Conduction is heat lost by direct contact with a cold
surface. It is exacerbated by moisture, either in the
environment (rain, snow, or water immersion) or in wet
clothing. Conduction can increase heat loss by up to 5
times with wet clothing and up to 25 times with water
immersion. Proper selection of clothing, footwear, layering, and activity level can drastically reduce conductive
heat losses. Subcutaneous fat stores also help to reduce
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conductive heat loss. Conductive and convective heat losses
usually account for approximately 15% of all heat losses;
however, high air speed, inadequate amounts of dry
clothing, wet clothing, and water immersion all drastically
increase conductive and convective heat losses.52
Evaporative heat losses account for 15% to 25% of the
total and occur through respiration and exposed skin.
Little can be done to reduce evaporative heat losses from
respiration, because ambient air must be warmed to core
temperature and humidified to 100% as it moves into the
respiratory tract. However, like conductive heat losses,
losses from the skin and sweating can be controlled
through proper selection of clothing and activity level.52
The amount of heat lost from the body can be calculated
using the classical heat balance equation. The equation
refers to the balancing of heat being produced by
metabolism (thermogenesis) and the rate at which it is
being lost to the environment via radiation, convection,
conduction, and evaporation (thermolysis). This equation
provides a conceptual understanding of the interplay
between the production of heat within the body and the
loss of heat to the environment. When an imbalance
develops between the rates of heat production and heat
loss, total body heat content changes.52 For example, when
an athlete ceases exercise, the level of heat production
diminishes, while the level of heat loss remains unchanged.
This leads to an imbalance between the rates of heat
production and heat loss.
S5M-R-C-K-E
S5heat gain/loss
M5metabolic heat production
R5radiative heat loss
C5convective heat loss
K5conductive heat loss
E5evaporative heat loss
Pathophysiology of Cold Injury
Hypothermia. Hypothermia (defined as a decrease in
core body temperature below 956F [356C]) can develop in
cold and dry or cold and wet conditions and can arise
either slowly over many hours or quite suddenly. Generally, slow-onset hypothermia occurs on land, whereas
sudden hypothermia results from cold-water immersion or
exposure to cold rain.1,7–9 The body loses heat faster than it
can generate heat and core temperature begins to drop.
Although we associate hypothermia with temperatures
below freezing, it also occurs at temperatures as high as
506F to 606F (106C–166C).3 For example, at the 1983
Bostonfest Marathon, 20% of the runners presenting for
treatment at the finish-line medical tent were diagnosed
with hypothermia3 despite an ambient temperature of
approximately 506F (106C). During the 1985 Boston
Marathon, 75 runners (1.3% of entrants) were treated for
hypothermia, even though the ambient temperature was
766F (246C).1
Hypothermia is caused by the body’s inability to
maintain a normal core temperature, with resulting
changes in the function of the nervous system, cardiovascular system, respiratory system, and renal system.62 The
central nervous system is susceptible to depression during
cold exposure. This depressed activity is typically manifested as changes in motor function (eg, clumsiness, loss of
finger dexterity, slurred speech), cognition (eg, confusion,
poor decision making, memory loss) and level of consciousness. Significant changes in central nervous system
function occur as core temperature drops below 956F
(356C), and show a linear decrease as core temperature
continues to drop. Brain function becomes measurably
abnormal below 92.36F (346C) and ceases at 666F to 686F
(196C–206C).7,62
Cardiovascular system functional change is manifested
as an initial tachycardia and then a progressive bradycardia
that decreases the resting heart rate by 50%. This drop in
heart rate is due to decreased depolarization of the heart
pacemaker cells. Other changes include increased myocardial oxygen demand and decreased arterial pressure and
cardiac output. The conduction system changes are
apparent during an electrocardiogram as prolonged PR,
QRS, and QT intervals. Additional arrhythmias may
include ventricular fibrillation and asystole, which can
occur when the core temperature is below 776F (256C), and
atrial fibrillation, which is common at core temperatures
below 89.66F (326C).7,62
The renal system responds to cold exposure by excreting
large amounts of glomerular filtrate. This cold-induced
diuresis appears to be due to a large increase in central
volume secondary to peripheral vasoconstriction. Diuresis
may occur to balance fluid levels as the central circulation
becomes overloaded. The urine produced is very dilute,
regardless of hydration status. Cold-water immersion can
further increase urine output by 3.5 times normal. These
renal responses occur during rest and light activity.7,62
The respiratory system reacts to cold exposure by
initially producing a hyperventilation response. After the
initial response, however, the ventilation rate progressively
decreases as core temperature drops, reaching 5 to 10
breaths per minute below a core temperature of 866F
(306C). Carbon dioxide production also decreases by up to
50%, which can lead to respiratory acidosis. These
respiratory responses occur during rest and light activity.7,62
Frostbite. The pathophysiology of deep frostbite (defined
as actual freezing of body tissues) typically consists of 3
distinct phases: frostnip, mild frostbite, and deep frostbite.
The frostnip, or prefreeze, phase occurs with superficial
skin cooling below 506F (106C), resulting in loss of
sensation, constriction of the microvasculature, plasma
leakage, and increased viscosity of vascular contents.65
Mild frostbite, or freeze-thaw phase, begins as skin
temperature drops below 286F (226C) and extracellular ice
crystals form. The location and rate of crystal formation
depends on the severity of the cold stress (combination of
air temperature, moisture presence, and wind). Water
migrates across the cell membrane, resulting in intracellular
dehydration and increased intracellular electrolyte concentrations. As the cell volume decreases, the cell eventually
collapses, the membrane ruptures, and cell death occurs.
As crystallization progresses, surrounding cells and vascular structures are compressed.65–67
The third phase, or severe frostbite, results in microvascular collapse at the arteriole and venule levels. As
microvascular tissue fails, blood viscosity increases, resulting in microthrombi, plasma leakage, increased tissue
pressure, ischemia, and tissue death. Nerve and muscle
tissue may also be affected. As edema resolves over
approximately 72 hours from onset, the most noticeable
sign of frostbite is gangrenous tissue.65–67
Blood flow to the skin of the extremities (acral skin) (eg,
fingers, toes, tip of nose) is under much stronger local
control of vasoconstriction and vasodilation than nonacral
skin and is very sensitive to local changes in temperature.
This local control is independent of the central nervous
system and produces significant changes in blood flow to
skin that is cooled, regardless of changes in core
temperature. Nonacral skin blood flow is controlled by
the central nervous system, and changes in flow are likely
due to changes in core temperature. These differences in
control of blood flow produce the scenario of potential
freezing injury to acral skin without a significant drop in
core body temperature.68
Chilblain (Pernio) and Immersion (Trench) Foot. Nonfreezing cold injuries, such as chilblain and immersion foot,
appear to share a common pathophysiology and generally
result in cellular damage without ice crystal formation.67
The abnormal inflammatory response typically leads to
intracellular and then extracellular fluid build-up. Increased extracellular fluid results in damage to neurologic
and vascular tissue. Classic symptoms of swelling, numbness, and itching, followed by hypersensitivity to cold after
rewarming, appear related to a dermal edema, migration of
lymph fluid, microvascular damage, and vascular and
neurologic hypersensitivity to cold exposure.67
Nonenvironmental Risk Factors
Health care providers should be aware of the following
nonenvironmental risk factors, which may make athletes
more susceptible to cold injury and may affect normal
physiologic responses to cold exposure.
Journal of Athletic Training
651
Previous Cold Injuries. Having sustained a previous cold
injury increases the chance of subsequent cold injuries by 2
to 4 times, even if prior injuries were not debilitating or
resolved with no or minimal medical care.3,6,69 For
example, an athlete who sustained frostnip or frostbite is
2 to 4 times more likely to develop frostbite in the same
area again, given similar environmental conditions.
Low Caloric Intake, Dehydration, and Fatigue. Low
caloric intake (less than 1200 to 1500 kcal/day) or
hypoglycemia (or both) directly decreases metabolism
and concomitant heat production,5 contributing to the
inability to maintain body temperature balance through
physical activity. Dehydration does not negatively affect
peripheral vasoconstriction or shivering and, therefore,
does not appear to increase susceptibility to cold injury.5,70–80 Fatigue associated with hypoglycemia is linked to
impaired peripheral vasoconstriction and shivering responses and can lead to faulty decision making and
inadequate preparations, indirectly resulting in cold
injuries.
Race. Black individuals have been shown to be 2 to 4
times more likely than individuals from other racial groups
to sustain cold injuries. These differences may be due to
cold weather experience, but are likely due to anthropometric and body composition differences, including lesspronounced CIVD, increased sympathetic response to cold
exposure, and thinner, longer digits.3,6
Nicotine, Alcohol, and Drug Use. Nicotine inhaled
through smoking causes a reflex peripheral vasoconstriction, possibly negating the CIVD and later enhancing the
cold-induced vasoconstriction to maintain core temperature. Alcohol reduces the glucose concentration in the
blood, which tends to decrease the shivering response.
Alcohol also may lead to faulty decision making due to its
effects on the central nervous system. Drugs with a
depressive effect may impair the thermoregulatory system
and so inhibit the body’s reaction to cold by blunting the
peripheral vasoconstriction and shivering responses. As with
alcohol, they may also lead to faulty decision making.77,81,82
Body Size and Composition. Body fat and muscle mass
appear to be instrumental in providing protection for
maintaining core body temperature with exposure to cold
air and water. This effect appears in both males and
females regardless of the amount of clothing worn. Strong
evidence suggests that percentage of body fat (.25%,
approximately) and amount of muscle mass are reliable
predictors of the ability to maintain and protect core body
temperature during prolonged exposure to a wide range of
cold air and water temperatures. The greater the level of
body fat and muscle mass, the better the ability to protect
core body temperature through passive (eg, insulative
properties of fat) and active (eg, shivering thermogenesis)
mechanisms.83–86
Aerobic Fitness Level and Training. Overall, physical
training and fitness level appear to have only minor
influence on thermoregulatory responses to cold. Most
cross-sectional comparisons of aerobically fit and less-fit
persons show no relationship between maximal aerobic
exercise capability and temperature regulation in the cold.
In those studies purportedly demonstrating a relationship,87,89 differences in thermoregulation appear more
likely attributable to anthropometric (body size and
composition) differences between aerobically fit and
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less-fit participants, rather than an effect of maximal
aerobic exercise capabilities per se. The primary thermoregulatory advantage provided by increased endurance
resulting from physical training is that a fitter individual
can sustain higher-intensity, longer-duration voluntary
activity than a less-fit person and, thus, maintain higher
sustained rates of metabolic heat production, keeping the
former warmer. In addition, exercise training has been
suggested to enhance the peripheral vasoconstriction
response, which would conserve body heat but possibly
increase peripheral cold injury risks.87–91
Sex. The hypothermia injury rate for females is 2 times
higher than for males. Sex differences in thermoregulatory
responses during cold exposure are influenced by interactions among total body fat content, subcutaneous fat
thickness, amount of muscle mass, and surface area-tomass ratio. For example, among men and women with
equivalent total body mass and surface areas, women’s
greater fat content enhances insulation and reduces the fall
in core temperature. In women and men of equivalent
subcutaneous fat thickness, women typically have a greater
surface area but smaller total body mass and smaller
muscle mass (thus, lower total body heat content) than men
and lose heat at a greater rate. Women’s thermogenic
response to cold exposure also appears less able to generate
metabolic heat than men of similar body composition due
to less total muscle mass. Therefore, total heat loss is
greater in women due to the larger surface area for
convective heat loss, and body temperature tends to fall
more rapidly for any given cold stress.91–94 As a result, the
prevention and recognition recommendations in this
position statement should be interpreted and used more
conservatively for female athletes than male athletes.
Clothing. The role of clothing in preventing cold injuries
lies in its ability to reduce heat loss to the environment by
trapping warm air. Cold-weather clothing typically has an
internal layer that allows evaporation of sweat without
absorption, a middle layer that provides insulation, and an
external layer that is wind and water resistant and allows
evaporation of moisture. The internal layer is in direct
contact with the skin and uses a moisture-wicking material
such as polyester or polypropylene. This layer should not
retain moisture but should transfer the moisture to other
layers, from which it can evaporate. The middle layer
provides the primary insulation against heat loss and can
be a fleece or wool material. The outer layer should have
venting abilities (eg, zippers or mesh in the armpits or low
back area) to allow moisture transfer to the environment.95
Clothing requirements for cold environment exercise
depend on ambient temperature; presence of wind, rain,
and water; and activity intensity. Generally speaking, as
exercise intensity increases at any given air temperature,
the amount of clothing insulation needed to maintain body
temperature equilibrium decreases. The insulative protection offered by different clothing combinations is represented in units of clo. One clo of insulation is the clothing
needed to permit a person to rest comfortably when the air
temperature is 706F (216C).96 See Table 4 for a list of the
clo values of common clothing combinations. Interactions
between exercise intensity and ambient conditions dictate
the selection of clothing based upon clo values. For
example, if the ambient temperature is 206F (276C) and
the person is at rest (1 metabolic equivalent of exercise
intensity), then clothing with a clo value of approximately 5
is needed to maintain core temperature. If activity is
increased to an exercise intensity of 4 metabolic equivalents, then clothing with a clo value of approximately 2
would be adequate.5 However, imposing a standard
clothing requirement for a group of individuals could
result in overheating in some and inadequate protection in
others. Individuals should be able to adjust clothing
according to their specific responses and comfort levels
while following general guidelines.
Other clothing considerations include the ability to
adapt when weather conditions change, especially if rain,
snow, or water immersion is a possibility. In these
instances, waterproof or water-resistant clothing should
be available, and the athlete should be able to change into
dry clothing as needed. Socks should not constrict blood
flow, should allow the evaporation of moisture, and should
be changed frequently after sweating or water immersion.
Another consideration is the heat lost from an uncovered
head. Even if the remainder of the body is well insulated in
ambient temperatures of 256F (246C),97 fleece, knit caps,
or other complete head coverings can significantly reduce
heat loss.
Predisposing Medical Conditions
The following medical conditions add to the risk of cold
injury or are exacerbated by exposure to cold environments.
Exercise-Induced Bronchospasm. Exercise-induced bronchospasm (EIB), also called exercise-induced asthma or
airway hyperresponsiveness, is a narrowing of the
respiratory tract airways. It is exacerbated by exposure
to cold, dry air. Predisposing factors include asthma and
allergies. However, not all individuals with EIB have
asthma or allergies, and not all individuals with asthma or
allergies have EIB. This condition can affect any
individual, from a small child at play to an elite
athlete.98–101 Authors102 have noted a high prevalence of
EIB in cold-weather athletes, in women, and in athletes
training and competing in indoor ice facilities. Two
possible mechanisms have been suggested to explain
EIB. The osmotic theory postulates that excessive airway
drying due to increased breathing rates enhances the
secretion of vasoconstrictor mediators in the breathing
passageways. This increased vasoconstrictor response
then limits air flow.103 A second theory suggests that the
combination of cold air and increased breathing rate cools
airways; after airways rewarm, increased blood flow leads
to edema formation and airway flow reductions.103 The
reduction of airway flow reduces maximal ventilation
and, subsequently, maximal performance.
Raynaud Syndrome. As with EIB, Raynaud syndrome is
caused by cold exposure and characterized by intermittent
vasospasm of the digital vessels. This vasospasm significantly
reduces blood flow to the extremities. The affected area may
present with tingling, swelling, or a throbbing pain. The skin
may turn a shade of white, then possibly blue, and then
becomes red upon rewarming. Raynaud syndrome describes
a spectrum of disorders whose causes are usually idiopathic,
although infrequently, autonomic dysfunction or an underlying condition such as thoracic outlet syndrome or collagen
vascular disease may be responsible.67
Anorexia Nervosa. Anorexia nervosa results in a
deficiency of body fat stores, potential malnutrition,
decreased metabolic rate, and peripheral vasoconstriction.
These changes limit the ability to maintain a normal core
temperature.104–106
Cold Urticaria. Cold urticaria may be the most common
form of urticaria.5,107 The condition has a rapid onset,
presenting with wheals (hives) that may be local or
generalized, redness, itching, and edema. Other symptoms
may include fatigue, headache, dyspnea, and in rare cases,
anaphylactic shock. Two forms of the condition, primary
acquired and secondary acquired (hereditary), have been
identified and differ in speed of onset: within minutes or 24
to 48 hours after cold exposure, respectively.107
Cardiovascular Disease. Individuals with cardiovascular
disease are sensitive to increased demands on the myocardium and increases in blood pressure, as well as having
potentially decreased flow to cutaneous and subcutaneous
tissues. Cold exposure coupled with exercise increases the
demand on the cardiovascular system by increased
sympathetic nervous system activity, peripheral resistance,
blood pressure, and myocardial oxygen demands. This
increased stress is in contrast to the demands of rest and
exercise in warm environments.108,109 Therefore, individuals with diminished cardiovascular system function should
be cautious when exercising in the cold and should be
monitored closely for symptoms associated with a myocardial infarction.
Environmental Risk Factors
Environmental cold stress results from a combination
of low air temperature; humidity, rain, or immersion; and
little thermal radiation and air movement. An index of
cold stress is the wind-chill temperature index (WCT)
(Figure 4). This index gives an indication of how cold a
person feels when exposed to a combination of cold air
and wind. This index estimates the danger of extreme
cooling of exposed skin (ie, the risk of frostbite) while
walking at 3 mph (1.3 m?s21) in various combinations of
conditions. When the WCT is below 2186F (2276C), the
risk of developing frostbite in exposed skin in less than
30 minutes increases, warranting closer observation.
However, the environmental wind speed in the WCT
does not account for wind produced during movement.
Biking or running produce wind across the body at the
same rate as body movement and should be taken into
account when estimating risk. For example, if a light wind
is present (less than 5 mph [2.24 m?s21]) with cold
temperatures (256F [246C]), the risk of frostbite for
most people is low. Yet if the athlete is cycling at 15 mph
(16.71 m?s21), the relative risk of developing frostbite
increases. Therefore, the effect of air movement produced
by the body should be taken into account when using the
wind-chill recommendations. The WCT is calculated
using the following formula27:
Wind chill (6F) 5 35.74 + 0.6215T 2 35.75V0.16 +
0.4275T(V0.16)
Where T 5 Air temperature (6F), and V 5 Wind speed
(mph)
This index is a useful tool to monitor the potential
thermal stress athletes must deal with when exposed to cold
temperatures.
Journal of Athletic Training
653
Influence of Wind, Rain, and Immersion
Exercise during windy or rainy conditions or water
immersion poses several unique challenges to the body’s
ability to maintain a normal body temperature. The
transfer of body heat in water may be 70 times greater
than in air.52 This transfer can lead to a significant loss of
body heat for those exercising in rainy conditions or in the
water. Maintaining normal body temperature in those
conditions depends on several factors, including exercise
intensity, exercise mode, anthropometric factors, insulative
properties of clothing and equipment, and the magnitude
of heat loss caused by wind speed, amount of rain, or water
temperature.52
During exercise in cold and wet conditions, the ability to
generate adequate metabolic heat to maintain body
temperature depends on exercise intensity and mode.51
More heat is lost from the arms and legs due to smaller
diameter and shorter distance from the limb center to the
surface, which allows rapid heat conduction compared with
the trunk. This increased conduction is outweighed when
exercise intensity is greater than 75% of maximal oxygen
uptake (V̇ O2 max).53,54 Exercise mode also affects the
ability to generate metabolic heat. The more muscle mass
involved in performing the exercise, the greater the heat
generated. Therefore, exercise involving only the lower
body generates more heat than exercise involving only the
upper body, and whole-body exercise generates more heat
than lower or upper body exercise alone.
The combination of windy and wet conditions can also
affect body temperature maintenance. Light to moderate
exercise in the rain leads to decreases in core temperature
compared with resting conditions.79 When air temperature
is 215.06F (56C) and clothes are wet, heat losses may
double those observed in dry conditions.55 Decreases in
core temperature have been observed with the addition of
wind during light-intensity exercise. With high-intensity
exercise (greater than 60% of peak oxygen consumption),
body temperature can be maintained in cold, windy, and
wet conditions.56
The influence of water temperature and amount of wet or
immersed skin also influences heat loss. The lower the water
temperature and the larger the surface area of the body
immersed in or in contact with water, the greater the heat
loss and the more rapid the decreases in core temperature.57
The best survival strategy for an individual exposed to
accidental, prolonged cold-water immersion (eg, boating or
water craft accident) has been debated: try to swim for
safety, move vigorously in place to generate body heat, or
remain quiet and move very little to conserve body heat.
Recent researchers110 suggested the following strategies:
1.
2.
3.
654
Stay calm. Unless you’re wearing an immersion suit,
you’ll experience cold shock when you go into cold
water due to rapid cooling of the skin. You won’t be
able to control your breathing, and you won’t get far if
you try to swim at this point. Your breathing will
return to normal in 2 to 3 minutes.
Make a plan. While you’re waiting for the cold shock
to subside, consider your situation and decide whether
to swim or stay in the present location.
If you decide to swim, look for the shore and decide if
you can make it. Most people studied could swim
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N Number 6 N December 2008
4.
5.
between 800 and 1500 m (874.9 and 1640.4 y) in cold
water, or for 45 minutes, before their arms and leg
muscles cooled to the point that they could no longer
swim.
If you decide to stay in place, try to get out of the
water as much as possible. Complete any tasks that
require the use of your hands, such as tying knots or
turning on flares, as soon as possible. As your hands
cool, they lose dexterity.
Stick to your decision; don’t change your mind midway.
After 30 minutes in cold water, you may become
hypothermic, and you won’t make the best decisions.
After immersion in cold water, athletes should be
monitored for the phenomenon of afterdrop. Once physical
activity concludes, the body still dissipates significant
amounts of heat but no longer generates metabolic heat
through activity. This imbalance between heat loss and
heat production could lead to drops in core temperature
during the rewarming process. Afterdrop is commonly
found in individuals after prolonged water immersion in
which core temperature has already decreased.30–32
Role of Cold Acclimatization. Cold acclimatization may
play a role in tolerance of cold exposure, but observed
adjustments are modest and rely upon the severity of
previous exposure. Adjustments found in persons with
recurring exposure to cold are habituation, metabolic
acclimatization, and insulative acclimatization.111
Cold-induced habituation manifests itself as a decreased
shivering and vasoconstriction response during cold
exposure compared with nonacclimatized exposures. Some
individuals may also have a greater decrease in core
temperature than nonacclimatized persons; this is known
as hypothermic habituation. Short, intense exposures that
occur a few times per week appear to elicit habituation.
Hypothermic habituation, however, occurs with longer
exposures in moderate temperatures during consecutive
days over a period greater than 2 weeks.111
Metabolic acclimatization is characterized by a more
pronounced shivering response to cold and typically occurs
after long-term exposures. Insulative acclimatization is
produced by greater conservation of heat during exposure
to cold. This includes a larger and more rapid decline in
skin temperature, resulting in less heat conduction at the
skin. Another response may be improved convective heat
loss due to a circulatory countercurrent heat exchange
mechanism.111
In comparison with the acclimatization observed with
repeated environmental heat exposure, adjustment to the
physiologic response during cold exposure appears to be
more difficult to acquire, varies more from individual to
individual, develops more slowly, and has less of a
preventive effect.
SPECIAL CONCERNS
Children (Prepubescents)
Exposure to cold environments poses unique challenges
for young athletes due to their higher surface area-to-mass
ratios and smaller adipose tissue deposits. These factors
result in a faster cooling rate than for adults in water and
similar cooling rates as adults in cold air. These rates
appear to be a function of a higher level of metabolic heat
production and a stronger peripheral vasoconstriction
response.112,113 Therefore, children should take similar
preventive measures as those suggested for adults, but they
should be encouraged to take more frequent breaks from a
cold environment, especially water immersion.
Older Individuals (More Than 50 Years Old)
As one ages, the ability to tolerate cold decreases and risk
of hypothermia increases.5,6 This increased risk for hypothermia appears to be due to diminished sympathetic
nervous system-mediated reflex vasoconstriction, which
allows greater heat loss.114 Additionally, an older individual
is more likely to have health concerns such as diabetes,
hypothyroidism, hypopituitarism, or hypertension, which
increase the likelihood of cold injury. As older individuals
continue an active lifestyle and as advances in medical and
surgical treatments extend life, more persons with histories of
myocardial infarction and stroke are becoming active in
outdoor environments.6,55,62,64,115,116 Thus, ATs working
with older athletes should apply prevention and recognition
recommendations more conservatively in this population.
Spinal Cord Injuries
The presence of a spinal cord injury (SCI) resulting in
some form of paralysis is associated with an increased risk
for hypothermia during cold exposure.117,118 Athletes with
SCI tend to be less sensitive to the sensation of cold on the
skin surface and have a diminished perception of skin
temperature change.119,120 Overall, individuals with SCI
have a diminished capability to stabilize core temperature121; specifically, they have a diminished autonomic
response to cold, which results in a decreased vasoconstriction response117,122 and a decreased effector response
to the muscle to generate metabolic heat.122 Those with
SCI also have abnormal blood pressure responses to cold
exposure,123 as well as increased complaints of muscle
spasticity, pain, and numbness.124–127 Consequently, athletes with SCI should be monitored closely for both core
temperature changes and skin changes associated with
nonfreezing cold injury.
CONCLUSIONS
Certified athletic trainers and other health care providers
must be able to identify the signs and symptoms of
hypothermia, frostbite, chilblains, and immersion (trench)
foot in athletes. This position statement outlines the current
recommendations to prevent the occurrence and improve the
recognition and treatment of cold injury in athletes.
ACKNOWLEDGMENTS
We gratefully acknowledge the efforts of Timothy S. Doane,
MA, ATC; Michael G. Dolan, MA, ATC; Ernie Hallbach, MA,
ATC; W. Larry Kenney, PhD; Glen P. Kenny, PhD; Roger
Kruse, MD; and the Pronouncements Committee in the
preparation of this document.
DISCLAIMER
The NATA publishes its position statements as a service to
promote the awareness of certain issues to its members. The
information contained in the position statement is neither
exhaustive not exclusive to all circumstances or individuals.
Variables such as institutional human resource guidelines, state or
federal statutes, rules, or regulations, as well as regional
environmental conditions, may impact the relevance and implementation of these recommendations. The NATA advises its
members and others to carefully and independently consider each
of the recommendations (including the applicability of same to
any particular circumstance or individual). The position statement should not be relied upon as an independent basis for care
but rather as a resource available to NATA members or others.
Moreover, no opinion is expressed herein regarding the quality of
care that adheres to or differs from NATA’s position statements.
The NATA reserves the right to rescind or modify its position
statements at any time.
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Thomas A. Cappaert, PhD, ATC, CSCS, CES, contributed to conception and design; analysis and interpretation of the data; and drafting,
critical review, and final approval of the article. Jennifer A. Stone, MS, ATC, CSCS, contributed to conception and design; analysis and
interpretation of the data; and drafting, critical revision, and final approval of the article. John W. Castellani, PhD, FACSM, contributed
to conception and design; analysis and interpretation of the data; and drafting, critical revision, and final approval of the article. Bentley
Andrew Krause, PhD, ATC, contributed to conception and design; analysis and interpretation of the data; and drafting, critical revision,
and final approval of the article. Daniel Smith, ATC, CSTS, ART, contributed to conception and design and critical revision and final
approval of the article. Bradford A. Stephens, MD, PC, contributed to conception and design and critical revision and final approval of the
article.
Address correspondence to National Athletic Trainers’ Association, Communications Department, 2952 Stemmons Freeway, Dallas, TX
75247.
658
Volume 43
N Number 6 N December 2008
Journal of Athletic Training 2000;35(4):471–477
© by the National Athletic Trainers’ Association, Inc
www.journalofathletictraining.org
National Athletic Trainers’ Association
Position Statement: Lightning Safety for
Athletics and Recreation
Katie M. Walsh, EdD, ATC-L*; Brian Bennett, MEd, ATC†;
Mary Ann Cooper, MD‡; Ronald L. Holle, MS§; Richard Kithil, MBA¶;
Raul E. López, PhD§
*East Carolina University, Greenville, NC; †The College of William and Mary, Williamsburg, VA; ‡The University of
Illinois at Chicago, Chicago, IL; §National Severe Storms Laboratory, Norman, OK; ¶The National Lightning Safety
Institute, Louisville, CO
Objective: To educate athletic trainers and others about the
dangers of lightning, provide lightning-safety guidelines, define
safe structures and locations, and advocate prehospital care
for lightning-strike victims.
Background: Lightning may be the most frequently encountered severe-storm hazard endangering physically active people each year. Millions of lightning flashes strike the ground
annually in the United States, causing nearly 100 deaths and
400 injuries. Three quarters of all lightning casualties occur
between May and September, and nearly four fifths occur
between 10:00 AM and 7:00 PM, which coincides with the hours
for most athletic or recreational activities. Additionally, lightning
casualties from sports and recreational activities have risen
alarmingly in recent decades.
Recommendations: The National Athletic Trainers’ Association recommends a proactive approach to lightning safety,
including the implementation of a lightning-safety policy that
identifies safe locations for shelter from the lightning hazard.
Further components of this policy are monitoring local weather
forecasts, designating a weather watcher, and establishing a
chain of command. Additionally, a flash-to-bang count of 30
seconds or less should be used as a minimal determinant of
when to suspend activities. Waiting 30 minutes or longer after
the last flash of lightning or sound of thunder is recommended
before athletic or recreational activities are resumed. Lightningsafety strategies include avoiding shelter under trees, avoiding
open fields and spaces, and suspending the use of land-line
telephones during thunderstorms. Also outlined in this document are the prehospital care guidelines for triaging and
treating lightning-strike victims. It is important to evaluate
victims quickly for apnea, asystole, hypothermia, shock, fractures, and burns. Cardiopulmonary resuscitation is effective in
resuscitating pulseless victims of lightning strike. Maintenance
of cardiopulmonary resuscitation and first-aid certification
should be required of all persons involved in sports and
recreational activities.
Key Words: lightning, policies and procedures, lightning
casualties, severe-storm hazards, environmental hazards,
emergency action plan, thunderstorms, lightning-safety policy,
athletics, recreation
O
States (Christoph Zimmerman, Global Atmospherics, Inc,
Tucson, AZ, unpublished data). Many of these strikes caused
fires, power outages, property damage, loss of life, and
disabling injuries. Property damage from lightning is estimated
to cost $5 000 000 000 to $6 000 000 000 annually in this
country.9 While print and television news reports of lightningstrike incidents to recreational athletes are frequent during the
thunderstorm season, many people are unsure about what to do
and where to go to improve their safety during thunderstorms.
It is incumbent on all individuals, particularly those who are
leaders in athletics and recreation, to appreciate the lightning
hazard, learn the published lightning-safety guidelines, and act
prudently, wisely, and in a spirit that will encourage safe
behavior in others.
The guidelines presented in this article govern all outdoor
activities, as well as indoor swimming-pool activities. The
purpose of this position statement is to recommend lightningsafety policy guidelines and strategies and to educate athletic
trainers and others involved with athletic or recreation activities about the hazards of lightning.
ver the past century, lightning has consistently been 1
of the top 3 causes of weather-related deaths in
this country.1,2 It kills approximately 100 people and
injures hundreds more each year.2–5 Lightning is an enormous
and widespread danger to the physically active population, due
in part to the prevalence of thunderstorms in the afternoon to
early evening during the late spring to early fall and a
societal trend toward outdoor physical activities.2,3,6 Certain
areas of the United States have higher propensities for thunderstorm activity, and thus, higher casualty rates: the Atlantic
seaboard, southwest, southern Rocky Mountains, and southern
plains states.2,7
Worldwide, approximately 2000 thunderstorms and 50 to
100 lightning flashes occur every second.8 In 1997, the
National Lightning Detection Network recorded nearly
27 000 000 cloud-to-ground lightning strikes in the United
Address correspondence to National Athletic Trainers’ Association,
Communications Department, 2952 Stemmons Freeway, Dallas, TX
75247.
Journal of Athletic Training
471
RECOMMENDATIONS
1. Formalize and implement a comprehensive, proactive
lightning-safety policy or emergency action plan specific
to lightning safety.1,7,10 –14 The components of this policy
should include the following:
A. An established chain of command that identifies who is
to make the call to remove individuals from the field or
an activity.
B. A designated weather watcher (ie, a person who actively
looks for the signs of threatening weather and notifies
the chain of command if severe weather becomes
dangerous).
C. A means of monitoring local weather forecasts and
warnings.
D. A listing of specific safe locations (for each field or site)
from the lightning hazard.
E. The use of specific criteria for suspension and resumption of activities (refer to recommendations 4, 5, and 6).
F. The use of the recommended lightning-safety strategies
(refer to recommendations 7, 8, and 9).
2. The primary choice for a safe location from the lightning
hazard is any substantial, frequently inhabited building.
The electric and telephone wiring and plumbing pathways
aid in grounding a building, which is why buildings are
safer than remaining outdoors during thunderstorms. It is
important not to be connected to these pathways while
inside the structure during ongoing thunderstorms.
3. The secondary choice for a safer location from the lightning hazard is a fully enclosed vehicle with a metal roof
and the windows closed.1,7,10,11,13,14 Convertible cars and
golf carts do not provide protection from lightning danger.
It is important not to touch any part of the metal framework of the vehicle while inside it during ongoing thunderstorms.
4. Seeking a safe structure or location at the first sign of
lightning or thunder activity is highly recommended. By
the time the flash-to-bang count approaches 30 seconds (or
is less than 30 seconds), all individuals should already be
inside or should immediately seek a safe structure or
location.1,13–15 To use the flash-to-bang method, the observer begins counting when a lightning flash is sighted.
Counting is stopped when the associated bang (thunder) is
heard. Divide this count by 5 to determine the distance to
the lightning flash (in miles). For example, a flash-to-bang
count of 30 seconds equates to a distance of 6 miles
(9.66 km).
5. Postpone or suspend activity if a thunderstorm appears
imminent before or during an activity or contest (regardless of whether lightning is seen or thunder heard) until the
hazard has passed. Signs of imminent thunderstorm activity are darkening clouds, high winds, and thunder or
lightning activity.
6. Once activities have been suspended, wait at least 30
minutes after the last sound of thunder or lightning
flash before resuming an activity or returning outdoors.1,13–15 A message should be read over the public
address system and lightning-safety tips should be placed
in game programs alerting spectators and competitors
about what to do and where to go to find a safer location
during thunderstorm activity.13,15
7. Extremely large athletic events are of particular concern with
regard to lightning safety. Consider using a multidisciplinary
472
Volume 35 • Number 4 • December 2000
8.
9.
10.
11.
12.
13.
approach to lessen lightning danger, such as integrating
weather forecasts, real-time thunderstorm data, a weather
watcher, and the flash-to-bang count to aid in decision
making.
Avoid being in contact with, or in proximity to, the highest
point of an open field or on the open water. Do not take
shelter under or near trees, flag poles, or light poles.1,8,10,13–15
Avoid taking showers and using plumbing facilities (including indoor and outdoor pools) and land-line telephones during
thunderstorm activity.1,8,10,13–15 Cordless or cellular telephones are safer to use when emergency help is needed.
Individuals who feel their hair stand on end or skin tingle or
hear crackling noises should assume the lightning-safe position (ie, crouched on the ground, weight on the balls of the
feet, feet together, head lowered, and ears covered). Do not lie
flat on the ground.1,8,10,13–15
Observe the following basic first-aid procedures, in order, to
manage victims of lightning strike16:
A. Survey the scene for safety. Ongoing thunderstorms may
still pose a threat to emergency personnel responding to
the situation.
B. Activate the local emergency management system.
C. Move the victim carefully to a safer location, if needed.
D. Evaluate and treat for apnea and asystole.
E. Evaluate and treat for hypothermia and shock.
F. Evaluate and treat for fractures.
G. Evaluate and treat for burns.
All persons should maintain current cardiopulmonary resuscitation (CPR) and first-aid certification.
All individuals should have the right to leave an athletic site
or activity, without fear of repercussion or penalty, in order to
seek a safe structure or location if they feel they are in danger
from impending lightning activity.13,15
BACKGROUND
Lightning-Flash Development
Within a developing thunderstorm cloud, updrafts promote
the collision of rising and descending ice and water particles,
and the positive and negative charges are separated into distinct
layers. Positive charges are taken via updrafts to the top of the
cloud, while negative charges accumulate in the bottom of the
cloud, creating the equivalent of a giant atmospheric battery.8
A cloud-to-ground lightning flash is the product of the
buildup and discharge of static electric energy between the
charged regions of the cloud and the earth. The negatively
charged lower region of the cloud induces a positive charge on
the ground below. The tremendous electric forces between
these 2 opposite charges initiate the lightning flash, which
begins as a barely visible step leader moving in a series of steps
downward from the cloud. Various objects on the ground
(trees, chimneys, people, etc) can produce positively charged,
upward streamers. The connection of the step leader with an
upward streamer determines the connection point on the
ground. After contact, a bright return stroke propagates upward
from the ground, while electrons move downward toward the
earth.8 This entire phenomenon happens in less than a fraction
of a second,8 but a large amount of charge is transferred to the
earth from the cloud.
Most lightning flashes have several return strokes, separated
by only 0.004 to 0.005 seconds.8 The human eye can barely
resolve the intervals between the strokes that cause the lightning flash to appear to flicker. A lightning flash is essentially
a brief spark, similar to that received from touching a doorknob
after walking across a carpeted room. The lightning channel is
approximately 2.54 cm (1 inch) in diameter and averages 4.83
to 8.05 km (3 to 5 miles) in vertical height but can be 9.66 km
(6 miles) or higher.8 Cloud-to-ground lightning flashes typically have peak currents ranging from 10 000 to 200 000 Å,
and the electric potential between the cloud and ground can be
10 000 000 to 100 000 000 V.8
Thunder is created when lightning quickly heats the air
around it, sometimes to temperatures greater than approximately 27 800°C (50 000°F), which is about 5 times hotter than
the surface of the sun.8 The rapidly heated air around a
lightning channel explodes, which in turn creates the sound we
hear as a clap of thunder.8 The audible range of thunder is
about 16.09 km (10 miles) but can be more or less depending
on local conditions.1 Heat lightning is intracloud or intercloud
lightning that is too distant for the accompanying thunder to be
heard.8 Although it is possible to have lightning without
thunder, thunder never occurs in the absence of lightning.
Lightning Casualty Demographics
On average, lightning kills approximately 100 people each
year in this country, while many hundreds more are injured.2–5
The death toll from lightning for 1940 to 1973 was greater than
that from tornadoes and hurricanes combined.17 Ninety-two
percent of lightning casualties occur between May and September, while July has the greatest number of casualties.2,3,7,18
Furthermore, 45% of the deaths and 80% of the casualties
occurred in these months between 10:00 AM and 7:00 PM,2,3,7,8
which coincides with the most likely time period for athletic or
recreational events. For these reasons, it is accurate to say that
lightning is the most dangerous and frequently encountered
severe-storm hazard that most people experience each
year.10,11
The statistics on lightning casualty demographics compiled
from the National Oceanographic and Atmospheric Administration publication Storm Data for the state of Colorado over
the last few decades demonstrate an increase in the number of
lightning casualties in persons involved in sports and outdoor
recreation.7,10,18,19 Fifty-two percent of lightning casualties
were people involved in outdoor recreation.7,18 In addition,
these authors noted that the highest number of casualties from
lightning was recorded in recreational and sports activities for
each year of the study.18 During the 1960s, more than 30% of
lightning casualties occurred during outdoor recreation activities; during the 1970s, that figure rose to 47%.17 Furthermore,
the rate of increase of lightning casualties during sports was
higher than the general United States population rate of
increase during the same time period.7,18
Lightning casualty statistics from Colorado demonstrate that
the most common sites for fatalities were open fields
(27%), near trees (16%), and close to water (13%).7,8,18
Statistics from the country as a whole mimic the numbers from
Colorado. Open fields, ballparks, and playgrounds accounted
for nearly 27% of casualties, and under trees (14%), waterrelated (8%), and golf-related (5%) deaths associated with
lightning followed.19 All these fatalities had 1 common denominator: being near the highest object or being the tallest
object in the immediate area. This single factor accounted for
56% of all fatalities from Colorado. Thus, it is imperative to
avoid high ridges and high points on the terrain, and conversely, it is important to seek low-lying points on the
terrain.1,3,8,13–15
The height above ground has been demonstrated to play a
prominent role in determining the strike probability. Therefore,
it is important to understand why minimizing vertical height is
critical in decreasing the chances of becoming a victim of
lightning. Warning signs of a high electromagnetic field and
imminent lightning strike include hair standing on end and
sounds similar to bacon sizzling or cloth tearing.8 If these
conditions occur, a cloud-to-ground lightning flash could strike
in the immediate area. Therefore, one should immediately
crouch in the lightning-safe position: feet together, weight on the
balls of the feet, head lowered, and ears covered.1 This position is
intended to minimize the probability of a direct strike by both
lowering the person’s height and minimizing the area in contact
with the surface of the ground. Taller objects are more likely to be
struck (but not always) because their upward streamer occurs first,
so that it is closer in proximity to the step leader coming
downward from the cloud.
The ultimate message is that individuals in dangerous
lightning situations should never wait to seek a safe location
and pursue safety measures. It is important to be proactive by
having all individuals inside a safe structure or location long
before the lightning is close enough to be threatening.
Mechanisms of Lightning Injury
Injury from lightning can occur via 5 mechanisms.16 A
direct strike most commonly occurs to the head, and lightning
current enters the orifices. This mechanism explains why eye
and ear injuries in lightning-strike victims are abundantly
reported in the literature.16 The shock wave created by the
lightning channel can also produce injuries, such as rupture of
the tympanic membrane, a common clinical presentation in the
lightning-strike victim.16,23,24 Recommending that individuals
cover their ears while in the lightning-safe position may help to
mitigate this type of injury.
The second mechanism, contact injury, occurs when the
lightning victim is touching an object that is in the pathway of
a lightning current.16 Side flash, the third mechanism, occurs
when lightning strikes an object near the victim and then jumps
from that object to the victim. This is the main danger to a
person who is sheltered under an isolated, tall tree.6 An upward
streamer is triggered by the tree but when this connects with
the step leader, the resulting stroke jumps to the victim, who
represents an additional pathway to ground.
The fourth mechanism, a step voltage or ground current,
occurs when the lightning current flowing in the ground
radiates outward in waves from the strike point. If 1 of the
individual’s feet is closer to the strike than the other, a step
voltage is created.6,16 Humans are primarily salt minerals in an
aqueous solution, and a lightning current preferentially travels
up from the earth through this solution (that is, the person)
rather than through the ground. The greater the differential step
voltage (ie, the greater the distance between the 2 feet), the
greater the likelihood of injury. Placing one’s feet close
together while in the crouched position and not lying flat on the
ground are crucial in reducing the likelihood of injury from a
step voltage or ground current.
Blunt injury is the fifth mechanism for lightning-strike
injuries. Lightning current can cause violent muscular contractions that throw its victims many meters from the strike point.
Journal of Athletic Training
473
Explosive and implosive forces created by the rapid heating
and cooling by the lightning current are also enough to produce
traumatic injuries.16
Common Effects of Lightning Injury
While lightning kills nearly 100 people annually in this
country, the protracted suffering of the survivors should not be
underestimated. Although the only acute cause of death
from lightning injury is cardiac arrest,20 the anoxic brain
damage that can occur if the person is not rapidly resuscitated
can be devastating. In addition, even for the survivor who did
not sustain a cardiac arrest, permanent sequelae can include
common brain-injury symptoms such as deficits in short-term
memory and processing of new information, as well as severe
and ongoing headaches, hyperirritability, sleep disturbances,
and distractibility.21,22 Others may develop chronic pain syndromes or absence-type seizures. Frequently, survivors are
unable to return to their previous level of function. They may
not be able to continue in their jobs or in their educational
pursuits and may be permanently disabled.
Components of a Lightning-Safety Policy
The purpose of formalizing a policy on lightning safety is to
provide written guidelines for safety during lightning storms.
Ninety-two percent of National Collegiate Athletic Association
Division I athletics departments responding to a survey did not
have a formal, written lightning-safety policy.12 The best
means of reducing the lightning hazard to people is to be
proactive. Athletic and recreational personnel should formalize and implement an emergency action plan specific to
lightning safety before the thunderstorm season.1,11,13–15
Dissemination of the plan is paramount, so that all persons
will know what to do and where to go to improve their own
safety during thunderstorms. The 6 components of a lightning-safety policy or emergency action plan for lightning
are discussed in the following paragraphs.
The first component in an emergency action plan or policy
for lightning safety is the establishment of a specific chain of
command that identifies the person who has the authority to
remove participants from athletic venues or activities. The
second is to appoint a weather watcher who actively looks for
signs of developing local thunderstorms, such as high winds,
darkening clouds, and any lightning or thunder.
The third element of a lightning-safety policy is the stipulation for monitoring local weather forecasts. One method is to
use weather radios that broadcast information on daily forecasts and approaching storm systems. Weather radios are an
excellent informational tool for general storm movement and
strength. While this information is extremely important in
decision making, the National Weather Service does not
broadcast information on specific storm cells or lightning.
Therefore, in addition to monitoring weather radios, it is
essential that the weather watcher be on constant lookout for
conditions in the immediate vicinity of the athletic event and
compare these conditions with the weather radio information.
When a local area is placed under a severe-storm watch or
warning by the National Weather Service, weather radios can
be programmed to give audible alert tones. A watch indicates
conditions are favorable for severe weather; a warning means
severe weather has been detected in the locale, and all persons
should take the necessary precautions to preserve their own
474
Volume 35 • Number 4 • December 2000
safety. If severe storms are in the vicinity, all individuals
should more intently monitor thunderstorm activity, such as
severity and direction of movement of the storm. It may also
mean that steps should be taken to remove athletes from the
field or perhaps to postpone or suspend athletic or recreational
activities during the event or before the storm begins.
Safe Locations
The fourth aspect of a lightning-safety policy, defining and
listing safe structures or locations to evacuate to in the event of
lightning, is of utmost importance. While there are reports of
people being injured by lightning inside buildings,8 evacuating
to a substantial building can considerably lower the risks of
lightning injury compared with those of remaining outside
during the thunderstorm. The lightning-safety policy should
identify the safe structure or location specific to each venue.
This information will enable individuals to know where to go
in advance of any thunderstorm situation and appreciate how
long it takes to get to the specific safe location from each field
or event site.
The primary choice for a safe structure is any fully enclosed,
substantial building.1,3,8,13–15 Ideally, the building should have
plumbing, electric wiring, and telephone service. The lightning
current is more likely to follow these pathways to ground,
which aids in electrically grounding the structure.8 If a substantial building is not available, a fully enclosed vehicle with
a metal roof and the windows completely closed is a reasonable
alternative.1,3,13–15 It is not the rubber tires that make the
vehicle safe but the metal enclosure that guides the lightning
current around the passengers, rather than through them. Do
not touch any part of the metal framework while inside the
vehicle.8 Convertible vehicles and golf carts do not provide a
high level of protection and cannot be considered safe from
lightning.
Unsafe Locations
Unfortunately, those properties that serve to define a safe
structure and improve the safety of its inhabitants also present
a potential risk. Lightning current can enter a building via the
electric or telephone wiring. It can also enter via a ground
current through the incoming plumbing pipelines. This condition makes locker-room shower areas, swimming pools (indoor
and outdoor), telephones, and electric appliances unsafe during
thunderstorms because of the possible contact with currentcarrying conduction. While such reports are rare, people have
been killed or injured by lightning in their homes while talking
on the telephone, taking a shower, or standing near household
appliances such as dishwashers, stoves, or refrigerators.1,3,8,13–15
From 1959 through 1965, lightning killed 4 people and
injured 36 others while they were talking on the telephone.
These numbers comprised 0.42% (n ⫽ 960) of deaths and 2.1%
(n ⫽ 1736) of injuries for the period.5 Studying reports from
Storm Data, researchers found that between 1959 and 1994,
2.4% of lightning casualties were telephone related.2 Because
they are not connected directly to a land-line phone, cellular
and cordless telephones are reasonably safe alternatives for
summoning help during a thunderstorm. It should be noted that
injury from acoustic damage can occur via explosive static
from the earpiece caused by a nearby lightning strike.
Even though a swimming pool may be indoors and apparently safe, it can be a dangerous location during thunderstorms.25 The current can be propagated through plumbing and
electric connections via the underwater lights and drains of
most swimming pools. Lightning current can also enter the
building, either into the electric wiring inside the building or
through underground plumbing pipelines that enter the building.8 If lightning strikes the building or ground nearby, the
current will most likely follow these pathways to the swimmers
through the water. Thus, indoor-pool activities are potentially
dangerous and should be avoided during thunderstorms.25
Small structures, such as rain or picnic shelters or athletic
storage sheds, are generally not properly protected and should
be avoided during thunderstorms. These locations may actually
increase the risk of lightning strike via a side flash and cause
injury to the occupants.
Criteria for Postponement and Resumption
of Activities
The fifth component of any lightning-safety policy is to
clearly describe criteria for both the suspension and resumption
of athletic or recreational activities. Various technologies
currently on the market propose to assist in determining when
lightning is in the immediate area. Within the developing area
of this lightning technology, data-based research is insufficient
to either support or dispute companies’ claims regarding
establishing when one is in danger of a lightning strike.
Therefore the National Athletic Trainers’ Association promotes the flash-to-bang standard to warn people of imminent
lightning danger. The flash-to-bang method is the easiest and
most convenient means for determining the distance to a
lightning flash and can also be used to determine when to
suspend or postpone activities. The flash-to-bang method is
based on the fact that light travels faster than sound, which
travels at a speed of approximately 1.61 km (1 mile) every 5
seconds.1,8,13,14 To use the flash-to-bang method, begin counting on the lightning flash, and stop counting when the
associated clap of thunder is heard. When storms have a high
flash rate, it is important to correlate a specific flash with the
thunder it produced. Divide the time to thunder (in seconds) by
5 to determine the distance (in miles) to the lightning
flash.1,8,13,14 For example, an observer obtains a count of 30
seconds from the time he or she spots the flash to when the
thunder is heard. Thirty divided by 5 equals 6; therefore, that
lightning flash was 6 miles (9.66 km) from the observer.
The 30-second rule is not an arbitrary guideline. López and
Holle26 studied storms in Oklahoma, Colorado, and Florida
and found that in larger thunderstorms, the distance between
successive flashes can be up to 6 miles (9.66 km) (ie, a
flash-to-bang count of 30 seconds) in approximately 80% of
the flash pairs. The authors also found the distance between
successive flashes may be as great as 9 miles (14.48 km) or
more, depending on local geography and atmospheric conditions. If a flash-to-bang count of 30 seconds is observed, the
next flash could conceivably be at the observer’s location.
Another important factor to consider when using the flashto-bang method is that, although a relatively rare occurrence,
lightning has been reported to strike 16.09 km (10 miles) or
more from where it is raining.1 Therefore, a flash-to-bang
count of at least 30 seconds is strongly recommended as a
determinant of when to suspend or postpone athletic or
recreational activities.13–15 As the flash-to-bang count ap-
proaches 30 seconds, all persons should be seeking, or already
inside, a safe structure or location. This is the minimal
guideline when using the flash-to-bang method to halt athletic
or recreational activities. Seeking a safe location at the first
sign of thunder or lightning activity is also highly recommended.
Another facet of the lightning-safety policy is embodied in
the “30 –30 rule” (Table 1), which relies on the flash-to-bang
method. If a game, practice, or other activity is suspended or
postponed due to lightning activity, it is important to establish
strict criteria in the lightning-safety policy for resumption of
activities. Waiting at least 30 minutes after the last lightning
flash or sound of thunder is recommended.13–15 When storm
reports and flash data at the time of death or injury were
compared, researchers found that the end of the storm, when
the flash-rate frequency began to decline, was as deadly as the
middle of the storm, when the lightning flash rate was at its
peak. The authors postulated that once the flash rate begins to
decline, people do not perceive the thunderstorm as dangerous
and are struck by lightning when they return outdoors prematurely.1 An important adage for athletic trainers, coaches, and
officials to remember is, “if you see it (lightning) flee it, if you
hear it (thunder), clear it.”
The 30-minute rule can also be explained in another way. A
typical thunderstorm moves at a rate of approximately 40.23
km (25 miles) per hour. Experts believe that 30 minutes allow
the thunderstorm to be about 16.09 to 19.31 km (10 to 12
miles) from the area, minimizing the probability of a nearby,
and therefore dangerous, lightning strike.15 Blue sky in the
local area or a lack of rainfall are not adequate reasons to
breach the 30-minute return-to-play rule. Lightning can strike
far from where it is raining, even when the clouds begin to
clear and show evidence of blue sky.1 This situation is often
referred to as a “bolt out of the blue.” Each time lightning is
observed or thunder is heard, the 30-minute clock should be
reset.
Obligation to Warn
The recommendation for reading lightning-safety messages
over public address systems and placing placards conspicuously around each venue resulted from a fatal lightning strike
in Washington, DC, in May 1991.27 During a high school
lacrosse game, a dangerous thunderstorm swept into the local
area, and the game was suspended. Lightning killed 1 young
person and injured 10 others who sought refuge under a tree.
Many people stated that they did not know what to do or where
to go to protect themselves from the dangers of lightning.
According to the basic principles of tort law, an individual
has a duty to warn others of dangers that may not be obvious
to a guest or subordinate of that person.28 Black et al29 defined
the legal principle of “foreseeability” as “the ability to see or
Table 1. The 30-30 Rule15
Criteria for suspension of
activities
Criteria for resumption of
activities
By the time the flash-to-bang
count approaches 30
seconds, all individuals should
already be inside a safe shelter.
Wait at least 30 minutes after
the last sound (thunder) or
observation of lightning before
leaving the safe shelter to
resume activities.
Journal of Athletic Training
475
know in advance, eg, reasonable anticipation, that harm or
injury is a likely result from certain acts or omissions.” With
regard to dangerous lightning situations, it could be argued that
an institution (or athletic department) has the duty to warn
spectators, invited guests, and participants if conditions are
such that lightning activity may be an imminent danger in the
immediate area. Whereas lightning is understood by all to be a
dangerous phenomenon, the importance of seeking safe shelter
and the specific time that one should vacate to safety are
generally not known. Based on research presented in this
article regarding the number of lightning casualties resulting
from the erroneous tendency of people to seek shelter under
trees, it would be wise for an organization to promote lightning
safety to its clientele and participants, including a list of
specific safe locations or structures.
Warnings should be commensurate with the age and understanding of those involved. Announcements should be repeated
over the public address system and colorful notices and safety
instructions both placed in the event programs and posted in
visible, high-traffic areas. Safety instructions should include
the location of the nearest safe shelter, similar to airline pocket
diagrams of nearest emergency exits. Being proactive with
regard to the lightning threat demands not putting individuals
at risk if a hazardous situation could have been prevented. If
thunderstorm activity looks menacing before or during an
event, consider canceling or postponing the event until the
complete weather situation can be ascertained and determined
to no longer be a threat. The first lightning flash from the
thunderstorm cloud and storms that produce only a few flashes
still pose a potential threat and should be treated as such. Every
cloud-to-ground lightning flash is dangerous and potentially
deadly and should not be taken lightly or viewed complacently.
Therefore, it is the recommendation of the National Athletic
Trainers’ Association to postpone or suspend athletic and
recreational activities before their onset, if thunderstorm activity appears imminent.
Prehospital Care of Victims
If a lightning-strike victim presents in asystole or respiratory
arrest, it is critical to initiate CPR as soon as safely possible.23 Because lightning-strike victims do not remain connected to a power source, they do not carry an electric charge
and are safe to assess.30 However, during an ongoing thunderstorm, lightning activity in the local area still poses a deadly
hazard for the medical team responding to the incident. The
athletic trainer or other medical personnel should consider his
or her own personal safety before venturing into a dangerous
situation to render care.
If medical personnel assume the risk of entering a dangerous
lightning situation to render care, the first priority should be to
move the victim to a safe location. In this way, a hazardous
situation can be neutralized for the athletic trainer, as well as
the victim. It is unlikely that moving a victim to an area of
greater safety for resuscitation will cause any serious injury to
the victim.16 The primary and secondary survey of the victim’s
condition can then be conducted once safety is reached.
It is not uncommon to find a lightning-strike victim unconscious, with fixed and dilated pupils and cold extremities and
in cardiopulmonary arrest. Case studies of individuals with
prolonged apnea and asystole after a lightning strike have
demonstrated successful resuscitations using CPR.23,24,31 Once
stopped, the heart will most likely spontaneously restart, but
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Volume 35 • Number 4 • December 2000
Table 2. Recommended Prehospital Care for Treating LightningStrike Victims16
Perform the following steps in order:
1. Survey the scene for safety.
2. Activate the local emergency management system.
3. Carefully move the victim to a safe area, if needed.
4. Evaluate and treat for apnea and asystole.
5. Evaluate and treat for hypothermia and shock.
6. Evaluate and treat for fractures.
7. Evaluate and treat for burns.
breathing centers in the brain may be damaged. Respiratory
arrest lasts longer than cardiac arrest, leading to secondary
asystole from hypoxia.16 Therefore, the basic principle of
triage, “treat the living first,” should be reversed in cases
involving casualties from a lightning strike. It is imperative to
treat those persons who are “apparently dead” first by promptly
initiating CPR. See Table 2 for quick-reference guidelines in
evaluating and treating victims of lightning strike.
CONCLUSIONS
Due to its pervasiveness during the times that most athletic
events occur, lightning is a significant hazard to the physically
active population. Lightning-casualty statistics show an alarming rise in the number of lightning casualties in recreational
and sports settings in recent decades.2,3,9 Each person must
take responsibility for his or her own personal safety during
thunderstorms.10 However, because people are often under the
direction of others, whether they are children or adults participating in organized athletics, athletic trainers, coaches, teachers, and game officials must receive education about the
hazards of lightning and become familiar with proved lightning-safety strategies. A policy is only as good as its compliance and unwavering, broad-based enforcement.
It is important to be much more wary of the lightning threat
than the rain. Lightning can strike in the absence of rain, as
well as from apparently clear blue skies overhead, even though
a thunderstorm may be nearby. The presence of lightning or
thunder should be the determining factor in postponing or
suspending games and activities, not the amount of rainfall on
the playing field. Lightning should be the only critical factor in
decision making for athletic trainers, umpires, officials, referees, and coaches.
Athletic trainers, umpires, officials, referees, coaches, teachers, and parents can make a difference in reducing the number
of lightning casualties if they (1) formalize and implement a
lightning-safety policy or emergency action plan specific to
lightning safety; (2) understand the qualifications of safe
structures or locations, in addition to knowing where they are
in relation to each athletic field or activity site; (3) understand
the 30 –30 rule as a minimal determinant of when to suspend
activities and follow it; being conservative and suspending
activities at the first sign of lightning or thunder activity is also
prudent and wise; (4) practice and follow the published
lightning-safety guidelines and strategies; (5) and maintain
CPR and standard first-aid certification.
ACKNOWLEDGMENTS
This position statement was reviewed for the National
Athletic Trainers’ Association by the Pronouncements Committee, Richard Ray, PhD, ATC, and Philip Krider, PhD.
REFERENCES
1. Holle RL, López RE, Howard KW, Vavrek J, Allsopp J. Safety in the
presence of lightning. Semin Neurol. 1995;15:375–380.
2. López RE, Holle RL, Heitkamp TA, Boyson M, Cherington M, Langford
K. The underreporting of lightning injuries and deaths in Colorado. Bull
Am Meteorol Soc. 1993;74:2171–2178.
3. Duclos PJ, Sanderson LM. An epidemiological description of lightningrelated deaths in the United States. Int J Epidemiol. 1990;19:673– 679.
4. Craig SR. When lightning strikes: pathophysiology and treatment of
lightning injuries. Postgrad Med. 1986;79:109 –112,121–123.
5. Zegel FH. Lightning deaths in the United States: a seven-year survey from
1959 to 1965. Weatherwise. 1967;20:169.
6. Andrews CJ, Cooper MA, Darveniza M. Lightning Injuries: Electrical,
Medical, and Legal Aspects. Boca Raton, FL: CRC Press; 1992.
7. López RE, Holle RL. Demographics of lightning casualties. Semin Neurol.
1995;15:286 –295.
8. Uman MA. All About Lightning. New York, NY: Dover Publications;
1986.
9. Kithil R. Annual USA lightning costs and losses. National Lightning
Safety Institute. Available at: www.lightningsafety.com/nlsi_lls/
nlsi_annual_usa_losses.htm. Accessed January 19, 1999.
10. Holle RL, López RE. Lightning: impacts and safety. World Meterol Bull.
1998;47:148 –155.
11. Holle RL, López RE, Vavrek J, Howard KW. Educating individuals about
lightning. In: Preprints of the American Meteorological Society 7th
Symposium on Education; January 11–16, 1998; Phoenix, AZ.
12. Walsh KM, Hanley MJ, Graner SJ, Beam D, Bazluki J. A survey of lightning
policy in selected Division I colleges. J Athl Train. 1997;32:206 –210.
13. Bennett BL. A model lightning safety policy for athletics. J Athl Train.
1997;32:251–253.
14. Bennett BL, Holle RL, López RE. Lightning safety guideline 1D. 1997–98
National Collegiate Athletic Association Sports Medicine Handbook. Overland Park, KS: National Collegiate Athletic Association; 1997–1998:12–14.
15. Vavrek JR, Holle RL, López RE. Updated lightning safety recommendations. In: Preprints of the American Meteorological Society 8th Symposium on Education; January 10 –15, 1999; Dallas, TX.
16. Cooper MA. Emergent care of lightning and electrical injuries. Semin
Neurol. 1995;15:268 –278.
17. Weigel EP. Lightning: the underrated killer. NOAA [National Oceanographic and Atmospheric Administration]. 1976;6:4 –11.
18. López RE, Holle RL, Heitkamp TA. Lightning casualties and property
damage in Colorado from 1950 to 1991 based on storm data. Weather
Forecast. 1995;10:114 –126.
19. Curran EB, Holle RL, López RE. Lightning Fatalities, Injuries, and
Damage Reports in the United States: 1959 –1994. Washington, DC:
National Oceanic and Atmospheric Administration; 1997. Technical
Memorandum NWS SR-193.
20. Cooper MA. Lightning: prognostic signs for death. Ann Emerg Med.
1980;9:134 –138.
21. Primeau M, Engelstatter GH, Bares KK. Behavioral consequences of
lightning and electrical injury. Semin Neurol. 1995;15:279 –285.
22. Andrews CJ, Darveniza M. Telephone-mediated lightning injury: an
Australian survey. J Trauma. 1989;29:665– 671.
23. Fontanarosa PB. Electrical shock and lightning strike. Ann Emerg Med.
1993;22(Pt 2):378 –387.
24. Steinbaum S, Harviel JD, Jaffin JH, Jordan MH. Lightning strike to the
head: case report. J Trauma. 1994;36:113–115.
25. Wiley S. Shocking news about lightning and pools. USA Swimming Safety
Q. 1998;4:1–2.
26. López RE, Holle RL. The distance between subsequent lightning flashes.
In: Preprints of the International Lightning Detection Conference;
November 17–18, 1998; Tucson, AZ.
27. Sanchez R, Wheeler L. Lightning strike at St. Albans game kills Bethesda
student, injures 10. Washington Post. May 18, 1991;A1.
28. Keeton WP, Dobbs DB, Keeton RE, Owen DG. Prosser and Keeton on
Torts. 5th ed. St. Paul, MN: West Publishing; 1984.
29. Black HC, Nolan JR, Nolan-Haley JM. Black’s Law Dictionary. 6th ed. St.
Paul, MN: West Publishing; 1990.
30. Cooper MA. Myths, miracles, and mirages. Semin Neurol. 1995;15:
358 –361.
31. Jepsen DL. How to manage a patient with lightning injury. Am J Nurs.
1992;92:38 – 42.
Journal of Athletic Training
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Journal of Athletic Training
2004;39(3):280–297
q by the National Athletic Trainers’ Association, Inc
www.journalofathletictraining.org
National Athletic Trainers’ Association
Position Statement: Management of SportRelated Concussion
Kevin M. Guskiewicz*; Scott L. Bruce†; Robert C. Cantu‡; Michael S.
Ferrara§; James P. Kelly\; Michael McCrea¶; Margot Putukian#;
Tamara C. Valovich McLeod**
*University of North Carolina at Chapel Hill, Chapel Hill, NC; †California University of Pennsylvania, California, PA;
‡Emerson Hospital, Concord, MA; §University of Georgia, Athens, GA; \University of Colorado, Denver, CO;
¶Waukesha Memorial Hospital, Waukesha, WI; #Princeton University, Princeton, NJ; **Arizona School of Health
Sciences, Mesa, AZ
Kevin M. Guskiewicz, PhD, ATC, FACSM; Scott L. Bruce, MS, ATC; Robert C. Cantu, MD, FACSM; Michael S. Ferrara, PhD,
ATC; James P. Kelly, MD; Michael McCrea, PhD; Margot Putukian, MD, FACSM; and Tamara C. Valovich McLeod, PhD, ATC,
CSCS, contributed to conception and design, acquisition and analysis and interpretation of the data; and drafting, critical
revision, and final approval of the article.
Address correspondence to National Athletic Trainers’ Association, Communications Department, 2952 Stemmons Freeway,
Dallas, TX 75247.
S
port in today’s society is more popular than probably
ever imagined. Large numbers of athletes participate in
a variety of youth, high school, collegiate, professional,
and recreational sports. As sport becomes more of a fixture in
the lives of Americans, a burden of responsibility falls on the
shoulders of the various organizations, coaches, parents, clinicians, officials, and researchers to provide an environment
that minimizes the risk of injury in all sports. For example,
the research-based recommendations made for football between 1976 and 1980 resulted in a significant reduction in the
incidence of fatalities and nonfatal catastrophic injuries. In
1968, 36 brain and cervical spine fatalities occurred in high
school and collegiate football. The number had dropped to
zero in 1990 and has averaged about 5 per year since then.1
This decrease was attributed to a variety of factors, including
(1) rule changes, which have outlawed spearing and butt
blocking, (2) player education about the rule changes and the
consequences of not following the rules, (3) implementation
of equipment standards, (4) availability of alternative assessment techniques, (5) a marked reduction in physical contact
time during practice sessions, (6) a heightened awareness
among clinicians of the dangers involved in returning an athlete to competition too early, and (7) the athlete’s awareness
of the risks associated with concussion.
Research in the area of sport-related concussion has provided the athletic training and medical professions with valuable
new knowledge in recent years. Certified athletic trainers, who
on average care for 7 concussive injuries per year,2 have been
forced to rethink how they manage sport-related concussion.
Recurrent concussions to several high-profile athletes, some of
whom were forced into retirement as a result, have increased
awareness among sports medicine personnel and the general
public. Bridging the gap between research and clinical practice
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• Number 3 • September 2004
is the key to reducing the incidence and severity of sportrelated concussion and improving return-to-play decisions.
This position statement should provide valuable information
and recommendations for certified athletic trainers (ATCs),
physicians, and other medical professionals caring for athletes
at the youth, high school, collegiate, and elite levels. The following recommendations are derived from the most recent scientific and clinic-based literature on sport-related concussion.
The justification for these recommendations is presented in the
summary statement following the recommendations. The summary statement is organized into the following sections: ‘‘Defining and Recognizing Concussion,’’ ‘‘Evaluating and Making the Return-to-Play Decision,’’ ‘‘Concussion Assessment
Tools,’’ ‘‘When to Refer an Athlete to a Physician After Concussion,’’ ‘‘When to Disqualify an Athlete,’’ ‘‘Special Considerations for the Young Athlete,’’ ‘‘Home Care,’’ and ‘‘Equipment Issues.’’
RECOMMENDATIONS
Defining and Recognizing Concussion
1. The ATC should develop a high sensitivity for the various
mechanisms and presentations of traumatic brain injury
(TBI), including mild, moderate, and severe cerebral concussion, as well as the more severe, but less common,
head injuries that can cause damage to the brain stem and
other vital centers of the brain.
2. The colloquial term ‘‘ding’’ should not be used to describe
a sport-related concussion. This stunned confusional state
is a concussion most often reflected by the athlete’s initial
confusion, which may disappear within minutes, leaving
no outwardly observable signs and symptoms. Use of the
term ‘‘ding’’ generally carries a connotation that diminishes the seriousness of the injury. If an athlete shows
concussion-like signs and reports symptoms after a contact to the head, the athlete has, at the very least, sustained
a mild concussion and should be treated for a concussion.
3. To detect deteriorating signs and symptoms that may indicate a more serious head injury, the ATC should be able
to recognize both the obvious signs (eg, fluctuating levels
of consciousness, balance problems, and memory and
concentration difficulties) and the more common, selfreported symptoms (eg, headache, ringing in the ears, and
nausea).
4. The ATC should play an active role in educating athletes,
coaches, and parents about the signs and symptoms associated with concussion, as well as the potential risks of
playing while still symptomatic.
5. The ATC should document all pertinent information surrounding the concussive injury, including but not limited
to (1) mechanism of injury; (2) initial signs and symptoms; (3) state of consciousness; (4) findings on serial testing of symptoms and neuropsychological function and
postural-stability tests (noting any deficits compared with
baseline); (5) instructions given to the athlete and/or parent; (6) recommendations provided by the physician; (7)
date and time of the athlete’s return to participation; and
(8) relevant information on the player’s history of prior
concussion and associated recovery pattern(s).3
Evaluating and Making the Return-to-Play Decision
6. Working together, ATCs and team physicians should agree
on a philosophy for managing sport-related concussion before the start of the athletic season. Currently 3 approaches
are commonly used: (1) grading the concussion at the time
of the injury, (2) deferring final grading until all symptoms have resolved, or (3) not using a grading scale but
rather focusing attention on the athlete’s recovery via
symptoms, neurocognitive testing, and postural-stability
testing. After deciding on an approach, the ATC-physician
team should be consistent in its use regardless of the athlete, sport, or circumstances surrounding the injury.
7. For athletes playing sports with a high risk of concussion,
baseline cognitive and postural-stability testing should be
considered. In addition to the concussion injury assessment, the evaluation should also include an assessment of
the cervical spine and cranial nerves to identify any cervical spine or vascular intracerebral injuries.
8. The ATC should record the time of the initial injury and
document serial assessments of the injured athlete, noting
the presence or absence of signs and symptoms of injury.
The ATC should monitor vital signs and level of consciousness every 5 minutes after a concussion until the
athlete’s condition improves. The athlete should also be
monitored over the next few days after the injury for the
presence of delayed signs and symptoms and to assess
recovery.
9. Concussion severity should be determined by paying close
attention to the severity and persistence of all signs and
symptoms, including the presence of amnesia (retrograde
and anterograde) and loss of consciousness (LOC), as well
as headache, concentration problems, dizziness, blurred
vision, and so on. It is recommended that ATCs and physicians consistently use a symptom checklist similar to the
one provided in Appendix A.
10. In addition to a thorough clinical evaluation, formal cognitive and postural-stability testing is recommended to assist in objectively determining injury severity and readiness to return to play (RTP). No one test should be used
solely to determine recovery or RTP, as concussion presents in many different ways.
11. Once symptom free, the athlete should be reassessed to
establish that cognition and postural stability have returned to normal for that player, preferably by comparison
with preinjury baseline test results. The RTP decision
should be made after an incremental increase in activity
with an initial cardiovascular challenge, followed by
sport-specific activities that do not place the athlete at risk
for concussion. The athlete can be released to full participation as long as no recurrent signs or symptoms are
present.
Concussion Assessment Tools
12. Baseline testing on concussion assessment measures is
recommended to establish the individual athlete’s ‘‘normal’’ preinjury performance and to provide the most reliable benchmark against which to measure postinjury recovery. Baseline testing also controls for extraneous
variables (eg, attention deficit disorder, learning disabilities, age, and education) and for the effects of earlier concussion while also evaluating the possible cumulative effects of recurrent concussions.
13. The use of objective concussion assessment tools will help
ATCs more accurately identify deficits caused by injury
and postinjury recovery and protect players from the potential risks associated with prematurely returning to competition and sustaining a repeat concussion. The concussion assessment battery should include a combination of
tests for cognition, postural stability, and self-reported
symptoms known to be affected by concussion.
14. A combination of brief screening tools appropriate for use
on the sideline (eg, Standardized Assessment of Concussion [SAC], Balance Error Scoring System [BESS], symptom checklist) and more extensive measures (eg, neuropsychological testing, computerized balance testing) to
more precisely evaluate recovery later after injury is recommended.
15. Before instituting a concussion neuropsychological testing
battery, the ATC should understand the test’s user requirements, copyright restrictions, and standardized instructions for administration and scoring. All evaluators should
be appropriately trained in the standardized instructions
for test administration and scoring before embarking on
testing or adopting an instrument for clinical use. Ideally,
the sports medicine team should include a neuropsychologist, but in reality, many ATCs may not have access to
a neuropsychologist for interpretation and consultation,
nor the financial resources to support a neuropsychological testing program. In this case, it is recommended that
the ATC use screening instruments (eg, SAC, BESS,
symptom checklist) that have been developed specifically
for use by sports medicine clinicians without extensive
Journal of Athletic Training
281
training in psychometric or standardized testing and that
do not require a special license to administer or interpret.
16. Athletic trainers should adopt for clinical use only those
neuropsychological and postural stability measures with
population-specific normative data, test-retest reliability,
clinical validity, and sufficient sensitivity and specificity
established in the peer-reviewed literature. These standards provide the basis for how well the test can distinguish between those with and without cerebral dysfunction in order to reduce the possibility of false-positive and
false-negative errors, which could lead to clinical decision-making errors.
17. As is the case with all clinical instruments, results from
assessment measures to evaluate concussion should be integrated with all aspects of the injury evaluation (eg, physical examination, neurologic evaluation, neuroimaging,
and player’s history) for the most effective approach to
injury management and RTP decision making. Decisions
about an athlete’s RTP should never be based solely on
the use of any one test.
When to Refer an Athlete to a Physician After
Concussion
18. The ATC or team physician should monitor an athlete
with a concussion at 5-minute intervals from the time of
the injury until the athlete’s condition completely clears
or the athlete is referred for further care. Coaches should
be informed that in situations when a concussion is suspected but an ATC or physician is not available, their
primary role is to ensure that the athlete is immediately
seen by an ATC or physician.
19. An athlete with a concussion should be referred to a physician on the day of injury if he or she lost consciousness,
experienced amnesia lasting longer than 15 minutes, or
meets any of the criteria outlined in Appendix B.
20. A team approach to the assessment of concussion should
be taken and include a variety of medical specialists. In
addition to family practice or general medicine physician
referrals, the ATC should secure other specialist referral
sources within the community. For example, neurologists
are trained to assist in the management of patients experiencing persistent signs and symptoms, including sleep
disturbances. Similarly, a neuropsychologist should be
identified as part of the sports medicine team for assisting
athletes who require more extensive neuropsychological
testing and for interpreting the results of neuropsychological tests.
21. A team approach should be used in making RTP decisions
after concussion. This approach should involve input from
the ATC, physician, athlete, and any referral sources. The
assessment of all information, including the physical examination, imaging studies, objective tests, and exertional
tests, should be considered prior to making an RTP decision.
exercises should include sideline jogging followed by
sprinting, sit-ups, push-ups, and any sport-specific, noncontact activities (or positions or stances) the athlete might
need to perform on returning to participation. Athletes
who return on the same day because symptoms resolved
quickly (,20 minutes) should be monitored closely after
they return to play. They should be repeatedly reevaluated
on the sideline after the practice or game and again at 24
and 48 hours postinjury to identify any delayed onset of
symptoms.
23. Athletes who experience LOC or amnesia should be disqualified from participating on the day of the injury.
24. The decision to disqualify from further participation on
the day of a concussion should be based on a comprehensive physical examination; assessment of self-reported
postconcussion signs and symptoms; functional impairments, and the athlete’s past history of concussions. If
assessment tools such as the SAC, BESS, neuropsychological test battery, and symptom checklist are not used,
a 7-day symptom-free waiting period before returning to
participation is recommended. Some circumstances, however, will warrant even more conservative treatment (see
recommendation 25).
25. Athletic trainers should be more conservative with athletes
who have a history of concussion. Athletes with a history
of concussion are at increased risk for sustaining subsequent injuries as well as for slowed recovery of self-reported postconcussion signs and symptoms, cognitive dysfunction, and postural instability after subsequent injuries.
In athletes with a history of 3 or more concussions and
experiencing slowed recovery, temporary or permanent
disqualification from contact sports may be indicated.
Special Considerations for the Young Athlete
26. Athletic trainers working with younger (pediatric) athletes
should be aware that recovery may take longer than in
older athletes. Additionally, these younger athletes are maturing at a relatively fast rate and will likely require more
frequent updates of baseline measures compared with older athletes.
27. Many young athletes experience sport-related concussion.
Athletic trainers should play an active role in helping to
educate young athletes, their parents, and coaches about
the dangers of repeated concussions. Continued research
into the epidemiology of sport-related concussion in
young athletes and prospective investigations to determine
the acute and long-term effects of recurrent concussions
in younger athletes are warranted.
28. Because damage to the maturing brain of a young athlete
can be catastrophic (ie, almost all reported cases of second-impact syndrome are in young athletes), athletes under age 18 years should be managed more conservatively,
using stricter RTP guidelines than those used to manage
concussion in the more mature athlete.
When to Disqualify an Athlete
Home Care
22. Athletes who are symptomatic at rest and after exertion
for at least 20 minutes should be disqualified from returning to participation on the day of the injury. Exertional
29. An athlete with a concussion should be instructed to avoid
taking medications except acetaminophen after the injury.
Acetaminophen and other medications should be given
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• Number 3 • September 2004
30.
31.
32.
33.
only at the recommendation of a physician. Additionally,
the athlete should be instructed to avoid ingesting alcohol,
illicit drugs, or other substances that might interfere with
cognitive function and neurologic recovery.
Any athlete with a concussion should be instructed to rest,
but complete bed rest is not recommended. The athlete
should resume normal activities of daily living as tolerated
while avoiding activities that potentially increase symptoms. Once he or she is symptom free, the athlete may
resume a graded program of physical and mental exertion,
without contact or risk of concussion, up to the point at
which postconcussion signs and symptoms recur. If symptoms appear, the exertion level should be scaled back to
allow maximal activity without triggering symptoms.
An athlete with a concussion should be instructed to eat
a well-balanced diet that is nutritious in both quality and
quantity.
An athlete should be awakened during the night to check
on deteriorating signs and symptoms only if he or she
experienced LOC, had prolonged periods of amnesia, or
was still experiencing significant symptoms at bedtime.
The purpose of the wake-ups is to check for deteriorating
signs and symptoms, such as decreased levels of consciousness or increasing headache, which could indicate a
more serious head injury or a late-onset complication,
such as an intracranial bleed.
Oral and written instructions for home care should be given to the athlete and to a responsible adult (eg, parent or
roommate) who will observe and supervise the athlete
during the acute phase of the concussion while at home
or in the dormitory. The ATC and physician should agree
on a standard concussion home-instruction form similar to
the one presented in Appendix C, and it should be used
consistently for all concussions.
Equipment Issues
34. The ATC should enforce the standard use of helmets for
protecting against catastrophic head injuries and reducing
the severity of cerebral concussions. In sports that require
helmet protection (football, lacrosse, ice hockey, baseball/
softball, etc), the ATC should ensure that all equipment
meets either the National Operating Committee on Standards for Athletic Equipment (NOCSAE) or American Society for Testing and Materials (ASTM) standards.
35. The ATC should enforce the standard use of mouth guards
for protection against dental injuries; however, there is no
scientific evidence supporting their use for reducing concussive injury.
36. At this time, the ATC should neither endorse nor discourage the use of soccer headgear for protecting against
concussion or the consequences of cumulative, subconcussive impacts to the head. Currently no scientific evidence supports the use of headgear in soccer for reducing
concussive injury to the head.
DEFINING AND RECOGNIZING CONCUSSION
Perhaps the most challenging aspect of managing sport-related concussion is recognizing the injury, especially in athletes with no obvious signs that a concussion has actually occurred. The immediate management of the head-injured athlete
depends on the nature and severity of the injury. Several terms
are used to describe this injury, the most global being TBI,
which can be classified into 2 types: focal and diffuse. Focal
or posttraumatic intracranial mass lesions include subdural hematomas, epidural hematomas, cerebral contusions, and intracerebral hemorrhages and hematomas. These are considered
uncommon in sport but are serious injuries; the ATC must be
able to detect signs of clinical deterioration or worsening
symptoms during serial assessments. Signs and symptoms of
these focal vascular emergencies can include LOC, cranial
nerve deficits, mental status deterioration, and worsening
symptoms. Concern for a significant focal injury should also
be raised if these signs or symptoms occur after an initial lucid
period in which the athlete seemed normal.
Diffuse brain injuries can result in widespread or global
disruption of neurologic function and are not usually associated with macroscopically visible brain lesions except in the
most severe cases. Most diffuse injuries involve an acceleration-deceleration motion, either within a linear plane or in a
rotational direction or both. In these cases, lesions are caused
by the brain being shaken within the skull.4,5 The brain is
suspended within the skull in cerebrospinal fluid (CSF) and
has several dural attachments to bony ridges that make up the
inner contours of the skull. With a linear acceleration-deceleration mechanism (side to side or front to back), the brain
experiences a sudden momentum change that can result in tissue damage. The key elements of injury mechanism are the
velocity of the head before impact, the time over which the
force is applied, and the magnitude of the force.4,5 Rotational
acceleration-deceleration injuries are believed to be the primary injury mechanism for the most severe diffuse brain injuries. Structural diffuse brain injury (diffuse axonal injury
[DAI]) is the most severe type of diffuse injury because axonal
disruption occurs, typically resulting in disturbance of cognitive functions, such as concentration and memory. In its most
severe form, DAI can disrupt the brain-stem centers responsible for breathing, heart rate, and wakefulness.4,5
Cerebral concussion, which is the focus of this position
statement, can best be classified as a mild diffuse injury and
is often referred to as mild TBI (MTBI). The injury involves
an acceleration-deceleration mechanism in which a blow to the
head or the head striking an object results in 1 or more of the
following conditions: headache, nausea, vomiting, dizziness,
balance problems, feeling ‘‘slowed down,’’ fatigue, trouble
sleeping, drowsiness, sensitivity to light or noise, LOC,
blurred vision, difficulty remembering, or difficulty concentrating.6 In 1966, the Congress of Neurological Surgeons proposed the following consensus definition of concussion, subsequently endorsed by a variety of medical associations:
‘‘Concussion is a clinical syndrome characterized by immediate and transient impairment of neural functions, such as
alteration of consciousness, disturbance of vision, equilibrium,
etc, due to mechanical forces.’’7 Although the definition received widespread consensus in 1966, more contemporary
opinion (as concluded at the First International Conference on
Concussion in Sport, Vienna, 20018) was that this definition
fails to include many of the predominant clinical features of
concussion, such as headache and nausea. It is often reported
that there is no universal agreement on the standard definition
or nature of concussion; however, agreement does exist on
several features that incorporate clinical, pathologic, and biomechanical injury constructs associated with head injury:
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283
1. Concussion may be caused by a direct blow to the head or
elsewhere on the body from an ‘‘impulsive’’ force transmitted to the head.
2. Concussion may cause an immediate and short-lived impairment of neurologic function.
3. Concussion may cause neuropathologic changes; however,
the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
4. Concussion may cause a gradient of clinical syndromes that
may or may not involve LOC. Resolution of the clinical
and cognitive symptoms typically follows a sequential
course.
5. Concussion is most often associated with normal results on
conventional neuroimaging studies.8
Occasionally, players sustain a blow to the head resulting
in a stunned confusional state that resolves within minutes.
The colloquial term ‘‘ding’’ is often used to describe this initial
state. However, the use of this term is not recommended because this stunned confusional state is still considered a concussion resulting in symptoms, although only very short in
duration, that should not be dismissed in a cavalier fashion. It
is essential that this injury be reevaluated frequently to determine if a more serious injury has occurred, because often the
evolving signs and symptoms of a concussion are not evident
until several minutes to hours later.
Although it is important for the ATC to recognize and eventually classify the concussive injury, it is equally important for
the athlete to understand the signs and symptoms of a concussion as well as the potential negative consequences (eg,
second-impact syndrome and predisposition to future concussions) of not reporting a concussive injury. Once the athlete
has a better understanding of the injury, he or she can provide
a more accurate report of the concussion history.
or stretching of tissue, whereas shearing involves a force that
moves across the parallel organization of the tissue. Brief, uniform compressive stresses are fairly well tolerated by neural
tissue, but tension and shearing stresses are very poorly tolerated.4,9
Neuroimaging of Cerebral Concussion
Traditionally, computed tomography (CT) and magnetic resonance imaging (MRI) have been considered useful in identifying certain types of brain lesions; however, they have been
of little value in assessing less severe head injuries, such as
cerebral concussion, and contributing to the RTP decision. A
CT scan is often indicated emergently if a focal injury such
as an acute subdural or epidural bleed is suspected; this study
easily demonstrates acute blood collection and skull fracture,
but an MRI is superior at demonstrating an isodense subacute
or chronic subdural hematoma that may be weeks old.10,11
Newer structural MRI modalities, including gradient echo, perfusion, and diffusion-weighted imaging, are more sensitive for
structural abnormalities (eg, vascular shearing) compared with
other diagnostic imaging techniques.10 Functional imaging
technologies (eg, positron emission tomography [PET], singlephoton emission computerized tomography [SPECT], and
functional MRI [fMRI]) are also yielding promising early results and may help define concussion recovery.12 Presently, no
neuroanatomic or physiologic measurements can be used to
determine the severity of a concussion or when complete recovery has occurred in an individual athlete after a concussion.
EVALUATING AND MAKING THE RETURN-TO-PLAY
DECISION
Clinical Evaluation
Mechanisms of Injury
A forceful blow to the resting, movable head usually produces maximum brain injury beneath the point of cranial impact (coup injury). A moving head hitting an unyielding object
usually produces maximum brain injury opposite the site of
cranial impact (contrecoup injury) as the brain shifts within
the cranium. When the head is accelerated before impact, the
brain lags toward the trailing surface, thus squeezing away the
CSF and creating maximal shearing forces at this site. This
brain lag actually thickens the layer of CSF under the point
of impact, which explains the lack of coup injury in the moving head. Alternatively, when the head is stationary before
impact, neither brain lag nor disproportionate distribution of
CSF occurs, accounting for the absence of contrecoup injury
and the presence of coup injury.4,5
No scientific evidence suggests that one type of injury (coup
or contrecoup) is more serious than the other or that symptoms
present any differently. Many sport-related concussions are the
result of a combined coup-contrecoup mechanism, involving
damage to the brain on both the side of initial impact and the
opposite side of the brain due to brain lag. Regardless of
whether the athlete has sustained a coup, contrecoup, or combined coup-contrecoup injury, the ATC should manage the injury the same.
Three types of stresses can be generated by an applied force
to injure the brain: compressive, tensile, and shearing. Compression involves a crushing force in which the tissue cannot
absorb any additional force or load. Tension involves pulling
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Results from a thorough clinical examination conducted by
both the ATC and the physician cannot be overlooked and
should be considered very important pieces of the concussion
puzzle. These evaluations should include a thorough history
(including number and severity of previous head injuries), observation (including pupil responses), palpation, and special
tests (including simple tests of memory, concentration, and
coordination and a cranial nerve assessment). In many situations, a physician will not be present at the time of the concussion, and the ATC will be forced to act on behalf of the
sports medicine team. More formal neuropsychological testing
and postural-stability testing should be viewed as adjuncts to
the initial clinical and repeat evaluations (see ‘‘Concussion Assessment Tools’’). The ATC-physician team must also consider
referral options to specialists such as neurologists, neurosurgeons, neuropsychologists, and neuro-otologists, depending on
the injury severity and situation. Referrals for imaging tests
such as CT, MRI, or electronystagmography are also options
that sometimes can aid in the diagnosis and/or management of
sport-related concussion but are typically used only in cases
involving LOC, severe amnesia, abnormal physical or neurologic findings, or increasing or intensified symptoms.
Determining Injury Severity
The definition of concussion is often expanded to include
mild, moderate, and severe injuries. Several early grading
scales and RTP guidelines early were proposed for classifying
and managing cerebral concussions.6,13–20 None of the scales
have been universally accepted or followed with much consistency by the sports medicine community. In addition, most
of these classification systems denote the most severe injuries
as associated with LOC, which we now know is not always
predictive of recovery after a brain injury.21,22 It is important
for the ATC and other health care providers to recognize the
importance of identifying retrograde amnesia and anterograde
amnesia, LOC, and other signs and symptoms present and to
manage each episode independently.
The ATC must recognize that no 2 concussions are identical
and that the resulting symptoms can be very different, depending on the force of the blow to the head, the degree of
metabolic dysfunction, the tissue damage and duration of time
needed to recover, the number of previous concussions, and
the time between injuries. All these factors must be considered
when managing an athlete suffering from cerebral concussion.3
The 2 most recognizable signs of a concussion are LOC and
amnesia; yet, as previously mentioned, neither is required for
an injury to be classified as a concussion. A 2000 study of
1003 concussions sustained by high school and collegiate football players revealed that LOC and amnesia presented infrequently, 9% and 27% of all cases, respectively, whereas other
signs and symptoms, such as headache, dizziness, confusion,
disorientation, and blurred vision, were much more common.23
After the initial concussion evaluation, the ATC should determine whether the athlete requires more advanced medical intervention on an emergent basis or whether the team physician
should be contacted for an RTP decision (Appendix B). It may
be helpful if the injury is graded throughout the process, but
this grading is likely to be more important for treating subsequent injuries than the current injury.
Most grading systems rely heavily on LOC and amnesia as
indicators of injury severity. Recent research, however, suggests that these 2 factors, either alone or in combination, are
not good predictors of injury severity. A number of authors
have documented no association between brief (,1 minute)
LOC and abnormalities on neuropsychological testing at 48
hours, raising concern for brief LOC as a predictor of recovery
after concussion.8,22,24–27 Studies involving high school and
collegiate athletes with concussion revealed no association between (1) LOC and duration of symptoms or (2) LOC and
neuropsychological and balance tests at 3, 24, 48, 72, and 96
hours postinjury.21,28,29 In other words, athletes experiencing
LOC were similar to athletes without LOC on these same injury-severity markers.
With respect to amnesia, the issue is more clouded because
findings have been inconsistent. Several studies of nonathletes30–37 suggest that the duration of posttraumatic amnesia
correlates with the severity and outcome of severe TBI but not
with mild TBI or concussion.38–40 More contemporary studies
of athletes with concussion are also clouded. Two unrelated,
prospective studies of concussion suggest that the presence of
amnesia best correlates with abnormal neuropsychological
testing at 48 hours and with the duration and number of other
postconcussion signs and symptoms.24,41 However, more recently, investigations of high school and collegiate athletes
with concussion revealed no association between (1) amnesia
and duration of symptoms or (2) amnesia and neuropsychological and balance tests at 3, 24, 48, 72, and 96 hours postinjury.21,28,29 Of importance in these studies is the significant
association between symptom-severity score (within the initial
3 hours postinjury) and the total duration of symptoms (mea-
Table 1. American Academy of Neurology Concussion Grading
Scale6
Grade 1 (mild)
Grade 2 (moderate)
Grade 3 (severe)
Transient confusion; no LOC*; symptoms
and mental status abnormalities resolve
,15 min
Transient confusion; no LOC; symptoms and
mental status abnormalities last .15 min
Any LOC
*LOC indicates loss of consciousness.
sured until asymptomatic). Although these findings suggest
that initial symptom severity is probably a better indicator than
either LOC or amnesia in predicting length of recovery, amnesia was recently found to predict symptom and neurocognitive deficits at 2 days postinjury.42 More research is needed
in this area to help improve clinical decision making.
It has been suggested that LOC and amnesia, especially
when prolonged, should not be ignored,43,44 but evidence for
their usefulness in establishing RTP guidelines is scarce. Loss
of consciousness, whether it occurs immediately or after an
initially lucid interval, is important in that it may signify a
more serious vascular brain injury. Other postconcussion signs
and symptoms should be specifically addressed for presence
and duration when the ATC is evaluating the athlete. Determining whether a cervical spine injury has occurred is also of
major importance because it is often associated with head injury and should not be missed. If the athlete complains of neck
pain or has cervical spine tenderness, cervical spine immobilization should be considered. If a cervical spine injury is ruled
out and the athlete is taken to the sideline, a thorough clinical
examination should follow, including a complete neurologic
examination and cognitive evaluation. The ATC must note the
time of the injury and then maintain a timed assessment form
to follow the athlete’s symptoms and examinations serially. It
is often difficult to pay attention to the time that has passed
after an injury. Therefore, it is important for one member of
the medical team to track time during the evaluation process
and record all pertinent information. After an initial evaluation, the clinician must determine whether the injured athlete
requires more advanced medical intervention and eventually
grade the injury and make an RTP decision that can occur
within minutes, hours, days, or weeks of the injury.
There are currently 3 approaches to grading sport-related
concussion. One approach is to grade the concussion at the
time of the injury on the basis of the signs and symptoms
present at the time of the concussion and within the first 15
minutes after injury. The American Academy of Neurology
Concussion Grading Scale (Table 1)6 has been widely used
with this approach. It permits the ATC to grade the injury
primarily on the basis of LOC and to provide the athlete,
coach, and parent with an estimation of injury severity. A disadvantage to this approach is that many injuries behave differently than expected on initial evaluation, potentially creating more difficulties with the athlete, coach, or parent and
making the RTP decision more challenging. Another approach
is to grade the concussion on the basis of the presence and
overall duration of symptoms. This approach is best addressed
using the Cantu Evidence-Based Grading Scale (Table 2),43
which guides the ATC to grade the injury only after all concussion signs and symptoms have resolved. This scale places
less emphasis on LOC as a potential predictor of subsequent
impairment and additional weight on overall symptom dura-
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285
Table 2. Cantu Evidence-Based Grading System for
Concussion43
Grade 1 (mild)
Grade 2 (moderate)
Grade 3 (severe)
No LOC*, PTA† ,30 min, PCSS‡ ,24 h
LOC ,1 min or PTA $30 min ,24 h or
PCSS $24 h ,7 d
LOC $1 min or PTA $24 h or PCSS $7 d
*LOC indicates loss of consciousness.
†PTA indicates posttraumatic amnesia (anterograde/retrograde).
‡PCSS indicates postconcussion signs and symptoms other than amnesia.
tion.3,43 Finally, a third approach to the grading-scale dilemma
is to not use a grading scale but rather focus attention on the
athlete’s recovery via symptoms, neuropsychological tests, and
postural-stability tests. This line of thinking is that the ATC
should not place too much emphasis on the grading system or
grade but should instead focus on whether the athlete is symptomatic or symptom free. Once the athlete is asymptomatic, a
stepwise progression should be implemented that increases demands over several days. This progression will be different for
athletes who are withheld for several weeks compared with
those athletes withheld for just a few days. This multitiered
approach was summarized and supported by consensus at the
2001 Vienna Conference on Concussion in Sport.8
Making the Return-to-Play Decision
The question raised most often regarding the concussion
grading and RTP systems is one of practicality in the sport
setting. Many clinicians believe that the RTP guidelines are
too conservative and, therefore, choose to base decisions on
clinical judgment of individual cases rather than on a general
recommendation. It has been reported that 30% of all high
school and collegiate football players sustaining concussions
return to competition on the same day of injury; the remaining
70% average 4 days of rest before returning to participation.23
Many RTP guidelines call for the athlete to be symptom free
for at least 7 days before returning to participation after a
grade 1 or 2 concussion.6,13,15,17,43,44 Although many clinicians deviate from these recommendations and are more liberal
in making RTP decisions, recent studies by Guskiewicz and
McCrea et al21,29 suggest that perhaps the 7-day waiting period
can minimize the risk of recurrent injury. On average, athletes
required 7 days to fully recover after concussion. Same-season
repeat injuries typically take place within a short window of
time, 7 to 10 days after the first concussion,21 supporting the
concept that there may be increased neuronal vulnerability or
blood-flow changes during that time, similar to those reported
by Giza, Hovda, et al45–47 in animal models.
Returning an athlete to participation should follow a progression that begins once the athlete is completely symptom
free. All signs and symptoms should be evaluated using a
graded symptom scale or checklist (described in ‘‘Concussion
Assessment Tools’’) when performing follow-up assessments
and should be evaluated both at rest and after exertional maneuvers such as biking, jogging, sit-ups, and push-ups. Baseline measurements of neuropsychological and postural stability
are strongly recommended for comparing with postinjury measurements. If these exertional tests do not produce symptoms,
either acutely or in delayed fashion, the athlete can then participate in sport-specific skills that allow return to practice but
should remain out of any activities that put him or her at risk
for recurrent head injury. For the basketball player, this may
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include shooting baskets or participating in walk-throughs, and
for the soccer player, this may include dribbling or shooting
drills or other sport-specific activities. These restricted and
monitored activities should be continued for the first few days
after becoming symptom free. The athlete should be monitored
periodically throughout and after these sessions to determine
if any symptoms develop or increase in intensity. Before returning to full contact participation, the athlete should be reassessed using neuropsychological and postural-stability tests
if available. If all scores have returned to baseline or better,
return to full participation can be considered after further clinical evaluation. It is strongly recommended that after recurrent
injury, especially within-season repeat injuries, the athlete be
withheld for an extended period of time (approximately 7
days) after symptoms have resolved.
CONCUSSION ASSESSMENT TOOLS
Sports medicine clinicians are increasingly using standardized methods to obtain a more objective measurement of postconcussion signs and symptoms, cognitive dysfunction, and
postural instability. These methods allow the clinician to quantify the severity of injury and measure the player’s progress
over the course of postinjury recovery. An emerging model of
sport concussion assessment involves the use of brief screening tools to evaluate postconcussion signs and symptoms, cognitive functioning, and postural stability on the sideline immediately after a concussion and neuropsychological testing to
track recovery further out from the time of injury. Ultimately,
these tests, when interpreted with the physical examination and
other aspects of the injury evaluation, assist the ATC and other
sports medicine professionals in the RTP decision-making process.
Data from objective measures of cognitive functioning, postural stability, and postconcussion signs and symptoms are
most helpful in making a determination about severity of injury and postinjury recovery when preinjury baseline data for
an individual athlete are available.3,8,24,29,41 Baseline testing
provides an indicator of what is ‘‘normal’’ for that particular
athlete while also establishing the most accurate and reliable
benchmark against which postinjury results can be compared.
It is important to obtain a baseline symptom assessment in
addition to baseline cognitive and other ability testing. Without
baseline measures, the athlete’s postinjury performance on
neuropsychological testing and other concussion assessment
measures must be interpreted by comparison with available
population normative values, which ideally are based on a
large sample of the representative population. Normative data
for competitive athletes on conventional (ie, paper-and-pencil)
and computerized neuropsychological tests and other concussion assessment measures are now more readily available from
large-scale research studies, but baseline data on an individual
athlete still provide the greatest clinical accuracy in interpreting postinjury test results. When performing baseline testing,
a suitable testing environment eliminates all distractions that
could alter the baseline performance and enhances the likelihood that all athletes are providing maximal effort. Most important, all evaluators should be aware of a test’s user requirements and be appropriately trained in the standardized
instructions for test administration and scoring before embarking on baseline testing or adopting a concussion testing paradigm for clinical use.
Several models exist for implementing baseline testing. Ide-
ally, preseason baseline testing is conducted before athletes are
exposed to the risk of concussion during sport participation
(eg, before contact drills during football). Some programs
choose to conduct baseline testing as part of the preparticipation physical examination process. In this model, stations
are established for various testing methods (eg, history collection, symptom assessment, neuropsychological testing, and
balance testing), and athletes complete the evaluation sequence
after being seen by the attending physician or ATC. This approach has the advantage of testing large groups of athletes in
1 session, while they are already in the mindset of undergoing
a preseason physical examination. When preseason examinations are not conducted in a systematic group arrangement,
alternative approaches can be considered. In any case, it is
helpful to conduct all modules of baseline testing on players
in 1 session to limit the complications of scheduling multiple
testing times and to keep testing conditions constant for the
athletes. One should allow adequate planning time (eg, 3
months) to implement a baseline testing module. Often this
equates to conducting baseline testing for fall sports during the
spring semester, before school is recessed for the summer. The
benefits of interpreting postinjury data for an athlete after a
concussion far outweigh the considerable time and human resources dedicated to baseline testing.
Collecting histories on individual athletes is also a vital part
of baseline testing, especially in establishing whether the athlete has any history of concussion, neurologic disorder, or other remarkable medical conditions. Specifically with respect to
concussion, it is important to establish (1) whether the player
has any history of concussions and, if so, how many and (2)
injury characteristics of previous concussions (eg, LOC, amnesia, symptoms, recovery time, time lost from participation,
and medical treatment). For athletes with a history of multiple
concussions, it is also important to clarify any apparent pattern
of (1) concussions occurring as a result of lighter impacts, (2)
concussions occurring closer together in time, (3) a lengthier
recovery time with successive concussions, and (4) a less complete recovery with each injury. Documenting a history of attentional disorders, learning disability, or other cognitive development disorders is also critical, especially in interpreting
an individual player’s baseline and postinjury performance on
neuropsychological testing. If resources do not allow for preseason examinations in all athletes, at least a concerted effort
to evaluate those athletes with a previous history of concussion
should be made because of the awareness of increased risk for
subsequent concussions in this group.
Postconcussion Symptom Assessment
Self-reported symptoms are among the more obvious and
recognizable ways to assess the effects of concussion. Typical
self-reported symptoms after a concussion include but are not
limited to headache; dizziness; nausea; vomiting; feeling ‘‘in
a fog’’; feeling ‘‘slowed down’’; trouble falling asleep; sleeping more than usual; fatigue; drowsiness; sensitivity to light
or noise; unsteadiness or loss of balance; feeling ‘‘dinged,’’
dazed, or stunned; seeing stars or flashing lights; ringing in
the ears; and double vision.8,26,48 Self-reported symptoms are
referenced by many of the concussion grading scales.10,43,44,49
The presence of self-reported symptoms serves as a major contraindication for RTP, and, based on current recommendations,
the athlete should be fully symptom free for at least 7 days at
rest and during exertion before returning to play.43,44
A number of concussion symptom checklists43,50–52 and
scales26,41,48,53 have been used in both research and clinical
settings. A symptom checklist that provides a list of concussion-related symptoms allows the athlete to report whether the
symptom is present by responding either ‘‘yes’’ (experiencing
the symptom) or ‘‘no’’ (not experiencing the symptom). A
symptom scale is a summative measure that allows the athlete
to describe the extent to which he or she is experiencing the
symptom. These instruments commonly incorporate a Likerttype scale that allows the player to rate the severity or frequency of postconcussion symptoms. These scores are then
summed to form a composite score that yields a quantitative
measure of overall injury severity and a benchmark against
which to track postinjury symptom recovery. Initial evidence
has been provided for the structural validity of a self-report
concussion symptom scale.48 Obtaining a baseline symptom
score is helpful to establish any preexisting symptoms attributable to factors other than the head injury (eg, illness, fatigue,
or somatization). Serial administration of the symptom checklist is the recommended method of tracking symptom resolution over time (see Appendix A).
Mental Status Screening
Cognitive screening instruments similar to the physician’s
mini mental status examination objectify what is often a subjective impression of cognitive abnormalities. Various methods
have been suggested for a systematic survey of mental status
and cognitive function in the athlete with a concussion. The
SAC was developed to provide sports medicine clinicians with
a brief, objective tool for assessing the injured athlete’s mental
status during the acute period after concussion (eg, sport sideline, locker room, and clinic).54 The SAC includes measures
of orientation, immediate memory, concentration, and delayed
recall that sum to 30 points.55 Lower scores on the SAC indicate more severe cognitive impairment. The SAC also includes assessments of strength, sensation, and coordination
and a standard neurologic examination but should not replace
the clinician’s thorough physical examination or referral for
more extensive neuropsychological evaluation when indicated.
Information about the occurrence and duration of LOC and
amnesia is also recorded on the SAC. Alternate forms of the
SAC are available to minimize the practice effects during retesting. The SAC takes about 5 minutes to administer and
should be used only after the clinician’s thorough review of
the training manual and instructional video on the administration, scoring, and interpretation of the instrument.
The SAC has demonstrated reliability29,55,56 and validi29,56,57
ty
in detecting mental status changes after a concussion.
Recent evidence suggests that a decline of 1 point or more
from baseline classified injured and uninjured players with a
level of 94% sensitivity and 76% specificity.56 The SAC is
also sensitive to detecting more severe neurocognitive changes
in injured athletes with LOC or amnesia associated with their
concussions.57 The SAC is most useful in the assessment of
acute cognitive dysfunction resulting from concussion, with
sensitivity and specificity comparable with extensive neuropsychological testing batteries during the initial 2 to 3 days
after concussion.29,58,59 As with neuropsychological testing,
sensitivity and specificity of the SAC in concussion assessment are maximized when individual baseline test data are
available.29,55,56,60
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287
Postural-Stability Assessment
A number of postural-stability tests have been used to assess
the effects of concussion in the clinical and laboratory settings.
The Romberg and stork stand were basic tests used to assess
balance and coordination. Riemann et al61–62 developed the
Balance Error Scoring System (BESS) based on existing theories of posturography. The BESS uses 3 stance positions and
tests on both a firm and a foam surface with the eyes closed
(for a total of 6 trials). The administration and scoring procedures are found in several publications.61–63 The BESS has
established good test-retest reliability and good concurrent validity when compared with laboratory forceplate measures52,62
and significant group differences, with an increased number of
errors for days 1, 3, and 5 postinjury when compared with
controls.52 Thus, the BESS can be used as a clinical measure
in identifying balance impairment that could indicate a neurologic deficit.
The NeuroCom Smart Balance Master System (NeuroCom
International, Clackamas, OR) is a forceplate system that measures vertical ground reaction forces produced by the body’s
center of gravity moving around a fixed base of support. The
Sensory Organization Test (SOT, NeuroCom International) is
designed to disrupt various sensory systems, including the visual, somatosensory, and vestibular systems. The SOT consists
of 6 conditions with 3 trials per condition, for a total of 18
trials, with each trial lasting 20 seconds. The complete administration has been described previously.52,64 The SOT has produced significant findings related to the assessment of concussion recovery. In a sample of 36 athletes with concussion, the
mean stability (composite score) and vestibular and visual ratios demonstrated deficits for up to 5 days postinjury.52 The
greatest deficits were seen 24 hours postinjury, and the athletes
with concussion demonstrated a gradual recovery during the
5-day period to within 6% of baseline scores. These results
were confirmed by Peterson et al,65 who found that these deficits continued for up to 10 days after concussion. These findings reveal a sensory interaction problem from the effects of
concussion with measurable changes in overall postural stability.
Neuropsychological Testing
Neuropsychological testing has historically been used to
evaluate various cognitive domains known to be preferentially
susceptible to the effects of concussion and TBI. In recent
years, neuropsychological testing to evaluate the effects of
sport-related concussion has gained much attention in the sport
concussion literature.20,21,26,29,48,52,58,59,65–69 The work of
Barth et al,70 who studied more than 2000 collegiate football
players from 10 universities, was the first project to institute
baseline neuropsychological testing. Similar programs are now
commonplace among many collegiate and professional teams,
and interest is growing at the high school level. Several recent
studies have supported the use of neuropsychological testing
as a valuable tool to evaluate the cognitive effects and recovery after sport-related concussion,24,28,29,41,42,50–52,57,65,66,71–75
but its feasibility for sideline use is not likely realistic. As is
the case with other concussion assessment tools, baseline neuropsychological testing is recommended, when possible, to establish a normative level of neurocognitive functioning for individual athletes. 24,28,29,41,50 –52,57–59,66,69,73–75 Baseline
neuropsychological testing typically takes 20 to 30 minutes per
athlete.
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Before implementing a neuropsychological testing program,
the ATC must consider several issues, including test-specific
training requirements and methodologic issues, the practicality
of baseline testing, the reliability and validity of individual
tests comprising the test battery, and the protocol for interpretation of the postinjury test results. Barr76 provided an excellent review on the methodologic and professional issues associated with neuropsychological testing in sport concussion
assessment. Most states require advanced training and licensure to purchase and use neuropsychological tests for clinical
purposes. Neuropsychological tests are also copyright protected to prevent inappropriate distribution or use by unqualified
professionals. At present, these requirements necessitate that a
licensed psychologist, preferably one Board certified in clinical
neuropsychology or with clinical experience in the evaluation
of sport-related concussion, oversee and supervise the clinical
application of neuropsychological testing for sport concussion
assessment. These factors likely restrict how widely neuropsychological testing can be used to assess sport-related concussion, especially at the high school level and in rural areas
where neuropsychologists are not readily available for consultation.
Neuropsychologists, ATCs, and sports medicine clinicians
are faced with the challenge of designing a model that jointly
upholds the testing standards of neuropsychology and meets
the clinical needs of the sports medicine community without
undue burden. The cost of neuropsychological testing, either
conventional or computerized, is also a factor in how widely
this method can be implemented, especially at the high school
level. Consultation fees for the neuropsychologist can be considerable if work is not done on a pro bono basis, and some
computerized testing companies charge a consulting fee for
interpreting postinjury test results by telephone.
Although no clear indications exist as to which are the best
individual neuropsychological tests to evaluate sport concussion, the use of multiple instruments as a ‘‘test battery’’ offers
clinicians greater potential for recognizing any cognitive deficits incurred from the injury. A number of neuropsychological
tests and test batteries have been used to assess sport-related
concussion. Table 3 provides a brief description of the paperand-pencil neuropsychological tests commonly used by neuropsychologists in the assessment of sport concussion. Sport
concussion batteries should include measures of cognitive abilities most susceptible to change after concussion, including
attention and concentration, cognitive processing (speed and
efficiency), learning and memory, working memory, executive
functioning, and verbal fluency. Tests of attention and concentration50,52,74,77 and memory functioning41 have been reported
as the most sensitive to the acute effects of concussion. The
athlete’s age, sex, primary language, and level of education
should be considered when selecting a test battery.68
Computerized Neuropsychological Tests. Recently, a
number of computerized neuropsychological testing programs
have been designed for the assessment of athletes after concussion. The Automated Neuropsychological Assessment Metrics (ANAM), CogSport, Concussion Resolution Index, and
Immediate Postconcussion Assessment and Cognitive Testing
(ImPACT) are all currently available and have shown promise
for reliable and valid concussion assessment (Table
4).24,41,51,53,66,71,72,75,78–84 The primary advantages to computerized testing are the ease of administration, ability to baseline
test a large number of athletes in a short period of time, and
multiple forms used within the testing paradigm to reduce the
Table 3. Common Neuropsychological Tests Used in Sport
Concussion Assessment
Neuropsychological Test
Controlled Oral Word Association
Test
Hopkins Verbal Learning Test
Trail Making: Parts A and B
Wechsler Letter Number Sequencing Test
Wechsler Digit Span: Digits Forward and Digits Backward
Wechsler Digit Symbol Test
Symbol Digit Modalities Test
Paced Auditory Serial Addition
Test
Stroop Color Word Test
Cognitive Domain
Verbal fluency
Verbal learning, immediate and
delayed memory
Visual scanning, attention, information processing speed, psychomotor speed
Verbal working memory
Attention, concentration
Psychomotor speed, attention,
concentration
Psychomotor speed, attention,
concentration
Attention, concentration
Attention, information processing
speed
practice effects. Collie et al71 summarized the advantage and
disadvantages of computerized versus traditional paper-andpencil testing.
As outlined, in the case of conventional neuropsychological
testing, several of the same challenges must be addressed before computerized testing becomes a widely used method of
sport concussion assessment. Issues requiring further consideration include demonstrated test reliability; validity, sensitivity, and specificity in the peer-reviewed literature; required
user training and qualifications; the necessary role of the licensed psychologist for clinical interpretation of postinjury
test results; hardware and software issues inherent to computerized testing; and user costs.71 Progress is being made on
many of these issues, but further clinical research is required
to provide clinicians with the most effective neuropsychological assessment tools and maintain the testing standards of neuropsychology.
Neuropsychological Testing Methods. Neuropsychological testing is not a tool that should be used to diagnose the
injury (ie, concussion); however, it can be very useful in measuring recovery once it has been determined that a concussion
has occurred. The point(s) at which postinjury neuropsychological testing should occur has been a topic of debate. A
variety of testing formats has been used to evaluate short-term
recovery from concussion.24,41,50,73,75,82 Two approaches are
most common. The first incorporates neuropsychological testing only after the injured player reports that his or her symptoms are completely gone. This approach is based on the conceptual foundation that an athlete should not participate while
symptomatic, regardless of neuropsychological test performance. Unnecessary serial neuropsychological testing, in addition to being burdensome and costly to the athlete and medical staff, also introduces practice effects that may confound
the interpretation of performance in subsequent postinjury testing sessions.85 The second approach incorporates neuropsychological testing at fixed time points (eg, postinjury day 1,
day 7, and so on) to track postinjury recovery. This approach
is often appropriate for prospective research protocols but is
unnecessary in a clinical setting when the player is still symptomatic and will be withheld from competition regardless of
the neuropsychological test results. In this model, serial testing
can be used until neuropsychological testing returns to normal,
preinjury levels and the player is completely symptom free.
Measuring ‘‘recovery’’ on neuropsychological tests and other clinical instruments is often a complex statistical matter,
further complicated by practice effects and other psychometric
dynamics affected by serial testing, even when preinjury baseline data are available for individual athletes. The use of statistical models that empirically identify meaningful change
while controlling for practice effects on serial testing may provide the clinician with the most precise benchmark in deter-
Table 4. Computerized Neuropsychological Tests
Neuropsychological Test
Developer (Contact Information)
Cognitive Domains
Automated Neuropsychological
Assessment Metrics (ANAM)
National Rehabilitation Hospital
Assistive Technology and
Neuroscience Center, Washington, DC84
(jsb2@mhg.edu)
Simple Reaction Metrics
Sternberg Memory
Math Processing
Continuous Performance
Matching to Sample
Spatial Processing
Code Substitution
CogSport
CogState Ltd, Victoria, Australia
(www.cogsport.com)
Simple Reaction Time
Complex Reaction Time
One-Back
Continuous Learning
Concussion Resolution
Index
HeadMinder Inc, New York, NY
(www.headminder.com)
Reaction Time
Cued Reaction Time
Visual Recognition 1
Visual Recognition 2
Animal Decoding
Symbol Scanning
Immediate Postconcussion Assessment
and Cognitive Testing (ImPACT)
University of Pittsburgh
Medical Center, Pittsburgh, PA
(www.impacttest.com)
Verbal Memory
Visual Memory
Information Processing Speed
Reaction Time
Impulse Control
Journal of Athletic Training
289
Table 5. Factors Influencing Neuropsychological Test
Performance68*
Previous concussions
Educational background
Preinjury level of cognitive functioning
Cultural background
Age
Test anxiety
Distractions
Sleep deprivation
Medications, alcohol, or drugs
Psychiatric disorders
Learning disability
Attention deficit/hyperactivity
Certain medical conditions
Primary language other than English
Previous neuropsychological testing
*Reprinted with permission of Grindel SH, Lovell MR, Collins MW. The
assessment of sport-related concussion: the evidence behind neuropsychological testing and management. Clin J Sport Med. 2001; 11:
134–143.
mining postinjury recovery, above and beyond the simple conclusion that the player is ‘‘back to baseline.’’ The complexity
of this analysis is the basis for the neuropsychologist overseeing the clinical interpretation of test data to determine injury
severity and recovery. Further research is required to clarify
the guidelines for determining and tracking recovery on specific measures after concussion. The clinician should also be
aware that any concussion assessment tool, either brief screening instruments or more extensive neuropsychological testing,
comes with some degree of risk for false negatives (eg, a player performs within what would be considered the normal range
on the measure before actually reaching a complete clinical
recovery after concussion). Therefore, test results should always be interpreted in the context of all clinical information,
including the player’s medical history. Also, caution should be
exercised in neuropsychological test interpretation when preinjury baseline data do not exist. Numerous factors apart from
the direct effects of concussion can influence test performance
(Table 5).
WHEN TO REFER AN ATHLETE TO A PHYSICIAN
AFTER CONCUSSION
Although most sport-related concussions are considered
mild head injuries, the potential exists for complications and
life-threatening injuries. Each ATC should be concerned about
the potential for the condition of an athlete with a concussion
to deteriorate. This downward trend can occur immediately
(minutes to hours) or over several days after the injury. As
discussed earlier, the spectrum of sport-related head injuries
includes more threatening injuries, such as epidural and subdural hematomas and second-impact syndrome. Postconcussion syndrome, however, is a more likely consequence of a
sport-related concussion. Not every sport-related concussion
warrants immediate physician referral, but ATCs must be able
to recognize those injuries that require further attention and
provide an appropriate referral for advanced care, which may
include neuroimaging. Serial assessments and physician follow-up are important parts of the evaluation of the athlete with
a concussion. Referrals should be made to medical personnel
with experience managing sport-related concussion. The ATC
should monitor vital signs and level of consciousness every 5
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• Number 3 • September 2004
minutes after a concussion until the athlete’s condition stabilizes and improves. The athlete should also be monitored over
the next few hours and days after the injury for delayed signs
and symptoms and to assess recovery. Appendix B outlines
scenarios that warrant physician referral or, in many cases,
transport to the nearest hospital emergency department.
WHEN TO DISQUALIFY AN ATHLETE
Return to participation after severe or repetitive concussive
injury should be considered only if the athlete is completely
symptom free and has a normal neurologic examination, normal neuropsychological and postural-stability examinations,
and, if obtained, normal neuroimaging studies (ie, MRI with
gradient echo). It may not be practical or even possible to use
all these assessments in all athletes or young children, but a
cautious clinical judgment should take into account all evaluation options. Each injured athlete should be considered individually, with consideration for factors including age, level
of participation, nature of the sport (high risk versus low risk),
and concussion history.
Standardized neuropsychological testing, which typically
assesses orientation, immediate and delayed memory recall,
and concentration may assist the ATC and physician in determining when to disqualify an athlete from further participation.60 Balance testing may provide additional information to
assist the clinician in the decision-making process of whether
to disqualify an individual after a concussion.52 When to disqualify the athlete is one of the most important decisions facing the ATC and team physician when dealing with an athlete
suffering from a concussion. This includes not only when to
disqualify for a single practice or event but also when to disqualify for the season or for a career.
Disqualifying for the Game or Practice
The decision to disqualify an individual from further participation on the day of the concussive episode is based on the
sideline evaluation, the symptoms the athlete is experiencing,
the severity of the apparent symptoms, and the patient’s past
history.86 The literature is clear: any episode involving LOC
or persistent symptoms related to concussion (headache, dizziness, amnesia, and so on), regardless of how mild and transient, warrants disqualification for the remainder of that day’s
activities.8,9,13,19,43,60,87 More recent studies of high school and
collegiate athletes underscore the importance of ensuring that
the athlete is symptom free before returning to participation
on the same day; even when the player is symptom free within
15 to 20 minutes after the concussive episode, he or she may
still demonstrate delayed symptoms or depressed neurocognitive levels. Lovell et al88 found significant memory deficits
36 hours postinjury in athletes who were symptom free within
15 minutes of a mild concussion. Guskiewicz et al21 found
that 33% (10/30) of the players with concussion who returned
on the same day of injury experienced delayed onset of symptoms at 3 hours postinjury, as compared with only 12.6% (20/
158) of those who did not return to play on the same day of
injury. Although more prospective work is needed in this area,
these studies raise questions as to whether the RTP criteria for
grade 1 (mild) concussions are conservative enough.
Disqualifying for the Season
Cantu43
Guidelines from
and the American Academy of
Neurology6 both recommend termination of the season after
the third concussion within the same season. The decision is
more difficult if one of the injuries was more severe or was a
severe injury resulting from a minimal blow, suggesting that
the athlete’s brain may be at particular risk for recurrent injury.
In addition, because many athletes participate in year-round
activities, once they are disqualified for the ‘‘season,’’ it may
be difficult to determine at what point they can resume contact
play. Other issues without clear-cut answers in the literature
are when to disqualify an athlete who has not been rendered
unconscious and whose symptoms cleared rapidly or one who
suffered multiple mild to moderate concussions throughout the
career and whether youth athletes should be treated differently
for initial and recurrent concussive injuries.
Disqualifying for the Career
When to disqualify an athlete for a career is a more difficult
question to answer. The duration of symptoms may be a better
criterion as to when to disqualify an athlete for the season or
longer. Merril Hoge, Eric Lindros, Chris Miller, Al Toon, and
Steve Young provide highly publicized cases of athletes sustaining multiple concussions with recurrent or postconcussion
signs and symptoms that lasted for lengthy periods of time.43
Once an athlete has suffered a concussion, he or she is at
increased risk for subsequent head injuries.21,43,86 Guskiewicz
et al21,23 found that collegiate athletes had a 3-fold greater risk
of suffering a concussion if they had sustained 3 or more previous concussions in a 7-year period and that players with 2
or more previous concussions required a longer time for total
symptom resolution after subsequent injuries.21 Players also
had a 3-fold greater risk for subsequent concussions in the
same season,23 whereas recurrent, in-season injuries occurred
within 10 days of the initial injury 92% of the time.21 In a
similar study of high school athletes, Collins et al82 found that
athletes with 3 or more prior concussions were at an increased
risk of experiencing LOC (8-fold greater risk), anterograde
amnesia (5.5-fold greater risk), and confusion (5.1-fold greater
risk) after subsequent concussion. Despite the increasing body
of literature on this topic, debate still surrounds the question
of how many concussions are enough to recommend ending
the player’s career. Some research suggests that the magic
number may be 3 concussions in a career.21,23,82 Although
these findings are important, they should be carefully interpreted because concussions present in varying degrees of severity, and all athletes do not respond in the same way to
concussive insults. Most important is that these data provide
evidence for exercising caution when managing younger athletes with concussion and athletes with a history of previous
concussions.
SPECIAL CONSIDERATIONS FOR THE YOUNG
ATHLETE
Many epidemiologic studies on concussion have focused on
professional or collegiate athletes. However, this focus seems
to now be shifting to the high school level and even to youth
sports. Special consideration must be given to the young athlete. The fact that the brain of the young athlete is still developing cannot be ignored, and the effect of concussion on
the developing brain is still not entirely understood. Even sub-
tle damage may lead to deficits in learning that adversely influence development. Therefore, it has been suggested that pediatric athletes suffering a concussion should be restricted
from further participation for the day and that additional consideration should be given as to when to return these individuals to activity.46
Recent epidemiologic investigations of head-injury rates in
high school athletes have shown that 13.3% of all reported
injuries in high school football affect the head and neck,
whereas the numbers in other sports range from 1.9% to 9.5%
in baseball and wrestling, respectively.89 Guskiewicz et al23
prospectively examined concussion incidence in high school
and collegiate football players and found that the greatest incidence was at the high school level (5.6%), compared with
the National Collegiate Athletic Association Division I (4.4%),
Division II (4.5%), and Division III (5.5%).
Authors who have tracked symptoms and neuropsychological function after concussion suggest that age-related differences exist between high school and collegiate athletes with
regard to recovery. Lovell et al41 reported that the duration of
on-field mental status changes in high school athletes, such as
retrograde amnesia and posttraumatic confusion, was related
to the presence of memory impairment at 36 hours, 4 days,
and 7 days postinjury as well as slower resolution of selfreported symptoms. These findings further emphasize the need
to collect these on-field measures after concussion and to use
the information wisely in making RTP decisions, especially
when dealing with younger athletes. Field et al90 found that
high school athletes who sustained a concussion demonstrated
prolonged memory dysfunction compared with collegiate athletes who sustained a concussion. The high school athletes
performed significantly worse on select tests of memory than
age-matched control subjects at 7 days postinjury when compared with collegiate athletes and their age-matched control
subjects. We hope these important studies and others will
eventually lead to more specific guidelines for managing concussions in high school athletes.
Very few investigators have studied sport-related injuries in
the youth population, and even fewer focused specifically on
sport-related concussion. One group91 reported that 15% of the
children (mean 5 8.34 6 5.31 years) who were admitted to
hospitals after MTBI suffered from a sport-related mechanism
of injury. Another group92 found that sport-related head injury
accounted for 3% of all sport-related injuries and 24% of all
serious head injuries treated in an emergency department. Additionally, sport-related concussion represented a substantial
percentage of all head injuries in children under the age of 10
years (18.2%) and 10- to 14-year-old (53.4%) and 15- to 19year-old (42.9%) populations.92 Thus, sport-related head injury has a relatively high incidence rate and is a significant
public health concern in youth athletes, not just participants at
higher competitive levels.
Although no prospective investigations in younger athletes
(younger than 15 years old) have been undertaken regarding
symptom resolution and cognitive or postural-stability recovery, Valovich McLeod et al93 recently determined the reliability and validity of brief concussion assessment tools in a
group of healthy young athletes (9–14 years old). The SAC is
valid within 48 hours of injury and reliable for testing of
youths above age 5 years, but younger athletes score slightly
below high school and collegiate athletes.55 This issue is remedied, however, if preseason baseline testing is conducted for
all players and a preinjury baseline score established for each
Journal of Athletic Training
291
athlete against which changes resulting from concussion can
be detected and other factors that affect test performance can
be controlled. Users of standardized clinical tools should be
aware of the effects of age and education on cognitive test
performance and make certain to select the appropriate normative group for comparison when testing an injured athlete
at a specific competitive level. Uncertainties about the effects
of concussion on young children warrant further study.
HOME CARE
Once the athlete has been thoroughly evaluated and determined to have sustained a concussion, a comprehensive medical management plan should be implemented. This plan
should include frequent medical evaluations and observations,
continued monitoring of postconcussion signs and symptoms,
and postinjury cognitive and balance testing. If symptoms persist or worsen or the level of consciousness deteriorates at all
after a concussion, neuroimaging should be performed. Although scientific evidence for the evaluation and resolution of
the concussion is ample, specific management advice to be
given to the athlete on leaving the athletic training room is
lacking.94 Athletic trainers and hospital emergency rooms have
created various home instruction forms, but minimal scientific
evidence supports these instructions. However, despite these
limitations, a concussion instruction form (Appendix C)
should be given to the athlete and a responsible adult who will
have direct contact with the athlete for the initial 24 hours
after the injury. This form helps the companion to know what
signs and symptoms to watch for and provides useful recommendations on follow-up care.
Medications
At this time, the clinician has no evidence-based pharmacologic treatment options for an athlete with a concussion.95
Most pharmacologic studies have been performed in severely
head-injured patients. It has been suggested that athletes with
concussion avoid medications containing aspirin or nonsteroidal anti-inflammatories, which decrease platelet function and
potentially increase intracranial bleeding, mask the severity
and duration of symptoms, and possibly lead to a more severe
injury. It is also recommended that acetaminophen (Tylenol,
McNeil Consumer & Specialty Pharmaceuticals, Fort Washington, PA) be used sparingly in the treatment of headachelike symptoms in the athlete with a concussion. Other substances to avoid during the acute postconcussion period
include those that adversely affect central nervous function, in
particular alcohol and narcotics.
Wake-Ups and Rest
Once it has been determined that a concussion has been
sustained, a decision must be made as to whether the athlete
can return home or should be considered for overnight observation or admission to the hospital. For more severe injuries,
the athlete should be evaluated by the team physician or emergency room physician if the team physician is not available.
If the athlete is allowed to return home or to the dormitory
room, the ATC should counsel a friend, teammate, or parent
to closely monitor the athlete. Traditionally, part of these instructions included a recommendation to wake up the athlete
every 3 to 4 hours during the night to evaluate changes in
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• Number 3 • September 2004
symptoms and rule out the possibility of an intracranial bleed,
such as a subdural hematoma. This recommendation has raised
some debate about unnecessary wake-ups that disrupt the athlete’s sleep pattern and may increase symptoms the next day
because of the combined effects of the injury and sleep deprivation. It is further suggested that the concussed athlete have
a teammate or friend stay during the night and that the athlete
not be left alone. No documented evidence suggests what severity of injury requires this treatment. However, a good rule
to use is if the athlete experienced LOC, had prolonged periods
of amnesia, or is still experiencing significant symptoms, he
or she should be awakened during the night. Both oral and
written instructions should be given to both the athlete and the
caregiver regarding waking.96 The use of written and oral instructions increases the compliance to 55% for purposeful
waking in the middle of the night. In the treatment of concussion, complete bed rest was ineffective in decreasing postconcussion signs and symptoms.97 The athlete should avoid
activities that may increase symptoms (eg, staying up late
studying and physical education class) and should resume normal activities of daily living, such as attending class and driving, once symptoms begin to resolve or decrease in severity.
As previously discussed, a graded test of exertion should be
used to determine the athlete’s ability to safely return to full
activity.
Diet
Evidence is limited to support the best type of diet for aiding
in the recovery process after a concussion. A cascade of neurochemical, ionic, and metabolic changes occur after brain injury.47 Furthermore, some areas of the brain demonstrate glycolytic increases and go into a state of metabolic depression
as a result of decreases in both glucose and oxidative metabolism with a reduction in cerebral blood flow. Severely braininjured subjects ate larger meals and increased their daily caloric intake when compared with controls.98 Although limited
information is available regarding the recommended diet for
the management of concussion, it is well accepted that athletes
should be instructed to avoid alcohol, illicit drugs, and central
nervous system medications that may interfere with cognitive
function. A normal, well-balanced diet should be maintained
to provide the needed nutrients to aid in the recovery process
from the injury.
EQUIPMENT ISSUES
Helmets and Headgear
Although wearing a helmet will not prevent all head injuries, a properly fitted helmet for certain sports reduces the risk
of such injuries. A poorly fitted helmet is limited in the amount
of protection it can provide, and the ATC must play a role in
enforcing the proper fitting and use of the helmet. Protective
sport helmets are designed primarily to prevent catastrophic
injuries (ie, skull fractures and intracranial hematomas) and
are not designed to prevent concussions. A helmet that protects
the head from a skull fracture does not adequately prevent the
rotational and shearing forces that lead to many concussions.99
The National Collegiate Athletic Association requires helmets be worn for the following sports: baseball, field hockey
(goalkeepers only), football, ice hockey, women’s lacrosse
(goalkeepers only), men’s lacrosse, and skiing. Helmets are
also recommended for recreational sports such as bicycling,
skiing, mountain biking, roller and inline skating, and speed
skating. Headgear standards are established and tested by the
National Operating Committee on Standards for Athletic
Equipment and the American Society for Testing and Materials.99
Efforts to establish and verify standards continue to be tested and refined, but rarely are the forces and conditions experienced on the field by the athletes duplicated. In addition to
direction, speed, and amount of the forces delivered and received by the athlete, conditions not controlled in the testing
process include weather conditions, changes in external temperatures and temperatures inside the helmet, humidity levels,
coefficient of friction for the surfaces of the equipment and
ground, and density of the equipment and ground. However,
equipment that does meet the standards is effective in reducing
head injuries.99
More recently, the issue of headgear for soccer players has
received much attention. Although several soccer organizations and governing bodies have approved the use of protective headbands in soccer, no published, peer-reviewed studies
support their use. Recommendations supporting the use and
performance of headgear for soccer are limited by a critical
gap in biomechanical information about head impacts in the
sport of soccer. Without data linking the severity and type of
impacts and the clinical sequelae of single and repeated impacts, specifications for soccer headgear cannot be established
scientifically. These types of headgear may reduce the ‘‘sting’’
of a head impact, yet they likely do not meet other sports
headgear performance standards. This type of headgear may
actually increase the incidence of injury. Players wearing
headgear may have the false impression that the headgear will
protect them during more aggressive play and thereby subject
themselves to even more severe impacts that may not be attenuated by the headgear.
Mouth Guards
The wearing of a mouth guard is thought by some to provide additional protection for the athlete against concussion by
either reducing the risk of injury or reducing the severity of
the injury itself.100 Mouth guards aid in the separation between
the head of the condyle of the mandible and the base of the
skull. It is thought that wearing an improperly fitted mouth
guard or none at all increases this contact point. This theory,
which is based on Newtonian laws of physics, suggests that
the increased separation between 2 adjacent structures increases the time to contact, thus decreasing the amount of contact
and decreasing the trauma done to the brain.100 However, no
biomechanical studies support the theory that the increased
separation results in less force being delivered to the brain.
High school football and National Collegiate Athletic Association football rules mandate the wearing of a mouth guard,
but the National Football League rulebook does not require
players to wear a mouth guard. The National Collegiate Athletic Association requires mouth guards to be worn by all athletes in football, field hockey, ice hockey, and lacrosse. Researchers 101,102 have found no advantage in wearing a
custom-made mouth guard over a boil-and-bite mouth guard
to reduce the rise of cerebral concussion in athletes. However,
ATCs and coaches should mandate the regular use of mouth
guards because a properly fitted mouth guard, with no alterations such as cutting off the back part, is of great value in
protecting the teeth and preventing fractures and avulsions that
could require many years of expensive dental care.
ACKNOWLEDGMENTS
We gratefully acknowledge the efforts of Kent Scriber, PhD, ATC;
Scott Anderson, MS, ATC; Michael Collins, PhD; Vito A. Perriello,
Jr, MD, PhD; Karen Johnston, MD, PhD; and the Pronouncements
Committee in the preparation of this document.
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Collins MW, Iverson GL, Lovell MR, McKeag DB, Norwig J, Maroon
J. On-field predictors of neuropsychological and symptom deficit following sports-related concussion. Clin J Sport Med. 2003;13:222–229.
Cantu RC. Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl
Train. 2001;36:244–248.
Kelly JP. Loss of consciousness: Pathophysiology and implications in
grading and safe return to play. J Athl Train. 2001;36:249–252.
Giza CC, Hovda DA. Ionic and metabolic consequences of concussion.
In: Cantu RC, ed. Neurologic Athletic Head and Spine Injuries. Philadelphia, PA: WB Saunders; 2000:80–100.
Giza CC, Hovda DA. The neurometabolic cascade of concussion. J Athl
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Hovda DA, Yoshino A, Kawamata T, Katayama Y, Becker DP. Diffuse
prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry
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Piland SG, Moti RW, Ferrara MS, Peterson CL. Evidence for the factorial and construct validity of a self-report concussion symptom scale.
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Guskiewicz KM. Concussion in sport: the grading-system dilemma. Athl
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50. Echemendia R, Putukian M, Mackin RS, Julian L, Shoss N. Neuropsychological test performance prior to and following sports-related mild
traumatic brain injury. Clin J Sport Med. 2001;11:23–31.
51. Erlanger D, Kaushik T, Cantu R, et al. Symptom-based assessment of
the severity of a concussion. J Neurosurg. 2003;98:477–484.
52. Guskiewicz KM, Ross SE, Marshall SW. Postural stability and neuropsychological deficits after concussion in collegiate athletes. J Athl
Train. 2001;36:263–273.
53. Collins MW, Field M, Lovell MR, et al. Relationship between postconcussion headache and neuropsychological test performance in high
school athletes. Am J Sports Med. 2003;31:168–173.
54. McCrea M. Standardized mental status assessment of sports concussion.
Clin J Sport Med. 2001;11:176–181.
55. McCrea M, Randolph C, Kelly JP. Standardized Assessment of Concussion (SAC): Manual for Administration, Scoring and Interpretation.
Waukesha, WI: CNS Inc; 1997.
56. Barr WB, McCrea M. Sensitivity and specificity of standardized neurocognitive testing immediately following sports concussion. J Int Neuropsychol Soc. 2001;7:693–702.
57. McCrea M, Kelly JP, Randolph C, Cisler R, Berger L. Immediate neurocognitive effects of concussion. Neurosurgery. 2002;50:1032–1042.
58. McCrea M, Kelly JP, Kluge J, Ackley B, Randolph C. Standardized
assessment of concussion in football players. Neurology. 1997;48:586–
588.
59. McCrea M, Kelly JP, Randolph C, et al. Standardized Assessment of
Concussion (SAC): on-site mental evaluation of the athlete. J Head
Trauma Rehabil. 1998;13:27–35.
60. McCrea M. Standardized mental status testing on the sideline after sportrelated concussion. J Athl Train. 2001;36:274–279.
61. Riemann BL, Guskiewicz KM. Effects of mild head injury on postural
stability as measured through clinical balance testing. J Athl Train. 2000;
35:19–25.
62. Riemann BL, Guskiewicz KM, Shields EW. Relationship between clinical and forceplate measures of postural stability. J Sport Rehabil. 1999;
8:71–62.
63. Valovich TC, Perrin DH, Gansneder BM. Repeat administration elicits
a practice effect with the Balance Error Scoring System but not with
the Standardized Assessment of Concussion in high school athletes. J
Athl Train. 2003;38:51–56.
64. Guskiewicz KM. Postural stability assessment following concussion: one
piece of the puzzle. Clin J Sport Med. 2001;11:182–189.
65. Peterson CL, Ferrara MS, Mrazik M, Piland SG. An analysis of domain
score and posturography following cerebral concussion. Clin J Sport
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66. Bleiberg J, Cernich AN, Cameron K, et al. Duration of cognitive impairment after sports concussion. Neurosurgery. 2004;54:1073–1080.
67. Bailes JE, Cantu RC. Head injury in athletes. Neurosurgery. 2001;48:
26–45.
68. Grindel SH, Lovell MR, Collins MW. The assessment of sport-related
concussion: the evidence behind neuropsychological testing and management. Clin J Sport Med. 2001;11:134–143.
69. Pottinger L, Cullum M, Stallings RL. Cognitive recovery following concussion in high school athletes. Arch Clin Neuropsychol. 1999;14:39–
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70. Barth JT, Alves WM, Ryan TV, et al. Mild head injury in sports: neuropsychological sequelae and recovery of function. In: Levin HS, Eisenberg HA, Benton AL, eds. Mild Head Injury. New York, NY: Oxford
University Press; 1989:257–275.
71. Collie A, Darby D, Maruff P. Computerised cognitive assessment of
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72. Collie A, Maruff P, Makdissi M, McCrory P, McStephen M, Darby D.
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73. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological performance in college football players.
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74. Macciocchi SN, Barth JT, Alves WM, Rimel RW, Jane JA. Neuropsy-
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35:354–360.
Barr WB. Methodologic issues in neuropsychological testing. J Athl
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Macciocchi SN, Barth JT, Littlefield LM. Outcome after mild head injury. Clin Sports Med. 1998;17:27–36.
Bleiberg J, Garmoe WS, Halpern EL, Reeves DL, Nadler JD. Consistency of within-day and across-day performance after mild brain injury.
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Bleiberg J, Halpern EL, Reeves D, Daniel JC. Future directions for the
neuropsychological assessment of sports concussion. J Head Trauma
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Bleiberg J, Kane RL, Reeves DL, Garmoe WS, Halpern E. Factor analysis of computerized and traditional tests used in mild brain injury research. Clin Neuropsychol. 2000;14:287–94.
Collie A, Maruff P, Darby DG, McStephen M. The effects of practice
on the cognitive test performance of neurologically normal individuals
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419–428.
Collins MW, Lovell MR, Iverson GL, Cantu RC, Maroon JC, Field M.
Cumulative effects of concussion in high school athletes. Neurosurgery.
2002;51:1175–1181.
Daniel JC, Olesniewicz MH, Reeves DL, et al. Repeated measures of
cognitive processing efficiency in adolescent athletes: implications for
monitoring recovery from concussion. Neuropsychiatry Neuropsychol
Behav Neurol. 1999;12:167–169.
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from sports related concussion? A comparison of high school and collegiate athletes. Am J Pediatr. 2003;142:546–553.
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and recreation-related head injuries treated in the emergency department.
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SJ, Gansneder BM. Serial administration of clinical concussion assessments and learning effects in healthy young athletes. Clin J Sport Med.
In press.
McCrory P. What advice should we give to athletes postconcussion? Br
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McCrory P. New treatments for concussion: the next millennium beckons. Clin J Sport Med. 2001;11:190–193.
de Louw A, Twijnstra A, Leffers P. Lack of uniformity and low compliance concerning wake-up advice following head trauma. Ned Tijdschr
Geneeskd. 1994;138:2197–2199.
de Kruijk JR, Leffers P, Meerhoff S, Rutten J, Twijnstra A. Effectiveness
of bed rest after mild traumatic brain injury: a randomised trial of no
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Halstead DP. Performance testing updates in head, face, and eye protection. J Athl Train. 2001;36:322–327.
Winters JE Sr. Commentary: role of properly fitted mouthguards in
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Labella CR, Smith BW, Sigurdsson A. Effect of mouthguards on
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Wisniewski JF, Guskiewicz KM, Trope M, Sigurdsson A. Incidence
of cerebral concussions associated with type of mouthguard used in
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Journal of Athletic Training
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Appendix A. Graded Symptom Checklist
296
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• Number 3 • September 2004
Appendix B. Physician Referral Checklist
Day-of-injury referral
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Loss of consciousness on the field
Amnesia lasting longer than 15 min
Deterioration of neurologic function*
Decreasing level of consciousness*
Decrease or irregularity in respirations*
Decrease or irregularity in pulse*
Increase in blood pressure
Unequal, dilated, or unreactive pupils*
Cranial nerve deficits
Any signs or symptoms of associated injuries, spine or skull
fracture, or bleeding*
11. Mental status changes: lethargy, difficulty maintaining arousal,
confusion, or agitation*
12. Seizure activity*
13. Vomiting
14.
15.
16.
17.
18.
19.
Motor deficits subsequent to initial on-field assessment
Sensory deficits subsequent to initial on-field assessment
Balance deficits subsequent to initial on-field assessment
Cranial nerve deficits subsequent to initial on-field assessment
Postconcussion symptoms that worsen
Additional postconcussion symptoms as compared with those on
the field
20. Athlete is still symptomatic at the end of the game (especially at
high school level)
Delayed referral (after the day of injury)
1.
2.
3.
4.
Any of the findings in the day-of-injury referral category
Postconcussion symptoms worsen or do not improve over time
Increase in the number of postconcussion symptoms reported
Postconcussion symptoms begin to interfere with the athlete’s
daily activities (ie, sleep disturbances or cognitive difficulties)
*Requires that the athlete be transported immediately to the nearest emergency department.
Appendix C. Concussion Home Instructions
I believe that
sustained a concussion on
. To make sure
he/she recovers, please follow the following important recommendations:
1. Please remind
to report to the athletic training room tomorrow at
for a follow-
up evaluation.
2. Please review the items outlined on the enclosed Physician Referral Checklist. If any of these problems develop prior to his/her visit, please
call
at
or contact the local emergency medical system or your family
physician. Otherwise, you can follow the instructions outlined below.
It is OK to:
There is NO need to:
Do NOT:
● Use acetaminophen (Tylenol)
for headaches
● Use ice pack on head and
neck as needed for comfort
● Eat a light diet
● Return to school
● Go to sleep
● Rest (no strenuous
activity or sports)
●
●
●
●
● Drink alcohol
● Eat spicy foods
Check eyes with flashlight
Wake up every hour
Test reflexes
Stay in bed
Specific recommendations:
Recommendations provided to:
Recommendations provided by:
Date:
Time:
Please feel free to contact me if you have any questions. I can be reached at:
Signature:
Date:
Journal of Athletic Training
297
Journal of Athletic Training
2011;46(2):206–220
g by the National Athletic Trainers’ Association, Inc
www.nata.org/jat
position statement
National Athletic Trainers’ Association Position
Statement: Prevention of Pediatric Overuse Injuries
Tamara C. Valovich McLeod, PhD, ATC*; Laura C. Decoster, ATC;
Keith J. Loud, MDCM, MSc`; Lyle J. Micheli, MD‰; J. Terry Parker, PhD, ATCI;
Michelle A. Sandrey, PhD, ATC"; Christopher White, MS, ATC#
*Athletic Training Program, A.T. Still University, Mesa, AZ; 3New Hampshire Musculoskeletal Institute, Manchester,
NH; 4Section of General Academic Pediatrics, Dartmouth-Hitchcock Medical Center, Lebanon, NH; 1Division of
Sports Medicine, Children’s Hospital, Boston, MA; IGwinnett Soccer Association, Lilburn, GA; "Graduate Athletic
Training Program, West Virginia University, Morgantown; #Brophy College Preparatory School, Phoenix, AZ
Objective: To provide certified athletic trainers, physicians,
and other health care professionals with recommendations on
best practices for the prevention of overuse sports injuries in
pediatric athletes (aged 6–18 years).
Background: Participation in sports by the pediatric population has grown tremendously over the years. Although the
health benefits of participation in competitive and recreational
athletic events are numerous, one adverse consequence is
sport-related injury. Overuse or repetitive trauma injuries
represent approximately 50% of all pediatric sport-related
injuries. It is speculated that more than half of these injuries
may be preventable with simple approaches.
Recommendations: Recommendations are provided based
on current evidence regarding pediatric injury surveillance,
identification of risk factors for injury, preparticipation physical
examinations, proper supervision and education (coaching and
medical), sport alterations, training and conditioning programs,
and delayed specialization.
Key Words: adolescents, children, chronic injuries, microtrauma, growth, development
O
be preventable,5 but few empirical data support this
statistic.
The purpose of this position statement is to provide
certified athletic trainers, physicians, and other health care
professionals with current best practice recommendations
regarding the prevention of overuse injuries in pediatric
athletes, including children (aged 6–12 years) and adolescents (aged 13–18 years).11 Even though specific age ranges
have been identified, it is important to note that the
occurrence of puberty, followed by skeletal maturity, is a
far more important marker of maturity than chronologic
age when managing pediatric overuse injuries. In particular, this position statement will provide recommendations
based on current evidence (Table 1) pertaining to injury
surveillance (eg, incidence, prevalence), identification of
risk factors for injury, preparticipation physical examinations (PPEs), proper supervision and education (coaching
and medical), sport alterations, training and conditioning
programs, and delayed specialization.
veruse injuries in the pediatric population represent
a significant health care concern. Some reports and
clinical observations1,2 indicate that 50% of pediatric patients present to sports medicine clinics for chronic
injuries. In addition to their costs (direct and indirect
medical expenditures), these injuries also result in lost
participation time, numerous physician visits, and lengthy
and often recurring rehabilitation.3–5 Furthermore, athletes
who sustain recurrent overuse injuries may stop participating in sports and recreational activities, thus potentially
adding to the already increasing number of sedentary
individuals and the obesity epidemic.
In the pediatric population, overuse injuries can include
growth-related disorders and those resulting from repeated microtrauma.6 Growth-related disorders include Osgood-Schlatter disease, Sever disease, and other apophyseal injuries. Overuse injuries resulting from repetitive
microtrauma and chronic submaximal loading of tissues
include stress fractures, similar to those described in adult
athletes.6 However, overlap exists between broad classifications; some growth-related disorders may occur in
sedentary children but much less often than in their
active peers.6 Regardless of the cause, these injuries can
result in significant pain and disability. Although little
research has identified causative factors for overuse
injuries in children and adolescents, these injuries may
be caused by training errors, improper technique,
excessive sports training, inadequate rest, muscle weakness and imbalances, and early specialization.6–10 More
than half of all reported overuse injuries are speculated to
206
Volume 46
N Number 2 N April 2011
RECOMMENDATIONS
Injury Surveillance
1.
Research should be devoted to improved understanding of the prevalence, incidence, and economic cost of
overuse injuries among pediatric athletes in the United
States and should focus on prevention and treatment
of these overuse injuries.12,13 Evidence Category: C
Table 1. Strength of Recommendation Taxonomy (SORT)a
Strength of
Recommendation
A
B
C
a
b
Definition
Recommendation based on consistent and good-quality patient-oriented evidenceb
Recommendation based on inconsistent or limited-quality experimental evidenceb
Recommendation based on consensus, usual practice, opinion, disease-oriented evidence,b or case series for studies of
diagnosis, treatment, prevention, or screening
Reprinted with permission from ‘‘Strength of Recommendation Taxonomy (SORT): A Patient-Centered Approach to Grading Evidence in the
Medical Literature,’’ February 1 2004, American Family Physician. g2004 American Academy of Family Physicians. All Rights Reserved.
Patient-oriented evidence measures outcomes that matter to patients: morbidity, mortality, symptom improvement, cost reduction, quality of life.
Disease-oriented evidence measures intermediate, physiologic, or surrogate end points that may or may not reflect improvements in patient
outcomes (ie, blood pressure, blood chemistry, physiological function, and pathological findings).
2.
3.
4.
Funding and support for research into the prevalence,
incidence, prevention, and treatment of pediatric
overuse injuries should be increased.12,13 Evidence
Category: C
All athletic health care providers should participate in
injury-surveillance efforts, including accurate documentation in keeping with good clinical practice, and
Web-based and other registries.12–14 Evidence Category: C
Resources and training for athletic health care
providers (eg, certified athletic trainer, physician,
physical therapist) to collect high-quality injury data
must be developed.12,13 Evidence Category: C
2. Decreasing the volume of pitches as a means to prevent
overuse injuries in throwing athletes is recommended.19–21 Evidence Category: A
3. Health care professionals should recognize that certain
anatomic factors may predispose the athlete to overuse
injury, including leg-length discrepancies, genu valgus,
genu varus, pelvic rotation, and generalized joint
hypermobility.9,10,22–24 Evidence Category: C
Coach Education and Medical Supervision
1.
Preparticipation Physical Examination
1.
2.
3.
4.
The PPE should be used as a means to screen each
athlete for potential risk factors, including injury
history, stature, maturity, joint stability, strength, and
flexibility, which may be important for preventing
recurrent injuries.5,6,15,16 Evidence Category: C
Children and adolescents with noted deficits on the
PPE should be referred to appropriate medical
specialists and health care providers (eg, physician
specialist, certified athletic trainer, physical therapist)
for further evaluation and corrective rehabilitation.5,15
Evidence Category: C
Robust documentation and injury-surveillance systems need to be developed to link PPE findings with
injury, thereby identifying which measured factors
may confer increased risk.14,17 Evidence Category: C
More research is needed to improve the effectiveness
of the PPE, including strategies to implement the
beneficial components more consistently and efficiently in the context of broader health-supervision and
morbidity-prevention efforts for adolescents.14,17 Evidence Category: C
2.
3.
4.
Sport Alterations
1.
Identification of Risk Factors
1. Arm pain, fatigue, and decreased throwing performance should be recognized by athletes, coaches,
parents, and medical personnel as early warning signs
of potential overuse injuries in pediatric throwers.18,19
Evidence Category: A
Pediatric athletes, parents, and coaches should be
educated about the signs and symptoms of overuse
injuries, and athletes should be instructed to notify an
adult when such symptoms occur.18,19,25 Evidence
Category: A
Coaches of youth and high school sports should have
certifications or credentials identifying specific knowledge in areas related to sports safety, sports techniques
and skills, psychosocial aspects of childhood and
adolescence, growth and development, and common
health and medical concerns.13,16,26,27 Evidence Category: C
Organized youth and interscholastic sports should be
supervised by adults, ideally those with knowledge and
training in monitoring for overuse injuries.5,13 Evidence Category: C
Medical personnel with training and education in
pediatric sports injuries should be identified as referral
sources to recognize, evaluate, and rehabilitate suspected overuse injuries.14,16Evidence Category: C
2.
Emerging evidence indicates that the sheer volume of
sport activity, whether measured as number of
throwing repetitions18–21,28 or quantity of time participating,29,30 is the most consistent predictor of overuse
injury. Efforts should be made to limit the total
amount of repetitive sport activity engaged in by
pediatric athletes to prevent or reduce overuse injuries.
Evidence Category: B
Although injury thresholds are yet to be determined
for specific activities and age ranges, some data
suggest a general guideline of no more than 16 to
Journal of Athletic Training
207
3.
4.
5.
6.
7.
20 hours per week of vigorous physical activity by
pediatric athletes.30 Evidence Category: B
Alterations or modifications to the existing rules for
adult sports may help to prevent overuse injuries in
pediatric athletes and should be considered by coaches
and administrators for sports in which youth rules are
lacking.5,13,31 Evidence Category: C
Adults should ensure that pediatric athletes play only 1
overhead throwing sport at a time, avoid playing that
sport year-round, and use caution when combining
pitching with other demanding throwing positions (eg,
pitch 1 day and catch the next day) to ensure adequate
time for recovery.7,28,32 Evidence Category: C
Parents and coaches should restrict the use of breaking
pitches in order to prevent pitching-related arm
injuries.20 If an individual pitcher can throw breaking
pitches on a limited basis and remain symptom free,
then it may be allowed; however, if the use of this pitch
precedes the development of any throwing-related
symptoms, it should be immediately terminated and
the athlete should seek medical attention. Evidence
Category: C
Pitching limits should be established for players 9 to
14 years old: full-effort throwing (ie, in competition)
should be limited to 75 pitches per game, 600 pitches
per season, and 2000 to 3000 pitches per year.20,33
Evidence Category: B
Pitchers between 15 and 18 years of age should throw
no more than 90 pitches per game and pitch no more
than 2 games per week.21,33Evidence Category: C
Training and Conditioning Programs
1.
2.
3.
4.
5.
208
Preseason and in-season preventive training programs
focusing on neuromuscular control, balance, coordination, flexibility, and strengthening of the lower
extremities are advocated for reducing overuse injury
risk, especially among pediatric athletes with a
previous history of injury.34–36 Evidence Category: A
All pediatric athletes should begin participating in a
general fitness program, emphasizing endurance,
flexibility, and strengthening, at least 2 months before
the sport season starts.5,9,37,38 Evidence Category: C
Pediatric athletes should have at least 1 to 2 days off
per week from competitive practices, competitions,
and sport-specific training.12,31 Coaches and administrators should consider these required days off when
organizing season schedules. Evidence Category: C
Pediatric athletes should participate on only 1 team of
the same sport per season when participation on 2 or
more teams of the same sport (eg, high school and
club) would involve practices or games (or both) more
than 5 days per week.31 Evidence Category: C
Progression of training intensity, load, time, and
distance should only increase by 10% each week to
allow for adequate adaptation and to avoid overload.5,31 Evidence Category: C
Volume 46
N Number 2 N April 2011
6.
After injury or delayed time without throwing,
pediatric throwing athletes should pursue a gradual
return-to-throwing program over several weeks before
beginning or resuming full throwing activities.7,32
Evidence Category: C
Delayed Specialization
1. Pediatric athletes should be encouraged to participate
in multiple sports and recreational activities throughout the year to enhance general fitness and aid in motor
development.5,13 Evidence Category: C
2. Pediatric athletes should take time off between sport
seasons and 2 to 3 nonconsecutive months away from a
specific sport if they participate in that sport yearround.31 Evidence Category: C
3. Pediatric athletes who participate in simultaneous (eg,
involvement in high school and club sports at the same
time) or consecutive seasons of the same sport should
follow the recommended guidelines with respect to the
cumulative amount of time or pitches over the year.31
Evidence Category: C
BACKGROUND AND LITERATURE REVIEW
Repetitive stress on the musculoskeletal system without
adequate and appropriate preparation and rest can result
in chronic or overuse injuries in athletes of any age. In
children and adolescents, this fact is complicated by the
growth process, which can result in a unique set of injuries
among pediatric athletes. Growth-related injuries most
frequently affect the epiphyseal plates, where long bone
growth occurs, and the apophyses, which serve as the bony
attachments for musculotendinous units.6 Compression is
usually responsible for epiphyseal injuries, whereas repeated tension or traction forces injure the apophyses.39
Differences in growth rates between the epiphyses and
apophyses and between bone and muscle tissue are factors
in apophyseal injury risk. These different growth rates may
lead to relative myotendinous inflexibility and increased
traction forces on the apophyses, contributing to traction
apophyseal injuries.40,41 In throwers, repetitive microtrauma can lead to further bony insult, resulting in capitellar
osteochondritis dissecans, a localized lesion of uncertain
cause that involves the separation of articular cartilage and
subchondral bone.42,43 Although most cases of osteochondritis dissecans resolve without consequence, lesions that
do not heal after surgical intervention or a period of
reduced repetitive impact loading may be responsible for
future sequelae, including degenerative changes.44
Growth-center injuries may have long-term physical
consequences and affect normal growth and development.16,40 However, little high-quality evidence supports
or refutes this suggestion. In a systematic review45 of
repetitive loading in gymnasts, females were at risk for
stress-related injuries of the distal radius, including distal
radial physeal arrest, but the lower-quality evidence of
most of the included studies limited the strength of
conclusions regarding whether physeal injury can inhibit
radial growth. In a more recent systematic review,16 12
studies of baseball pitchers (3 case series, 9 case studies)
with acute or chronic physeal injuries related to organized
sport were analyzed. Stress-related changes were reported
in all studies, including physeal widening in 8 reports,
osteochondritis and radiographic widening of the proximal
humeral growth plate in 2 reports, and humeral physis in 1
report.16 Most of these patients improved with rest and
were able to return to baseball, although some did not
continue to pitch.
Data from lower extremity physeal injury studies were
also extracted for review. Ten studies16 of lower extremity
physeal injury revealed that these injuries occurred mainly
in runners, but soccer, tennis, baseball (catcher), and
gymnastics athletes also showed radiographic changes of
physeal widening. Among the 17 studies (11 case reports, 6
case series) of physeal injury in gymnasts, traumatic
physeal arrest was described in 1, stress changes or fractures in 6, physeal widening in 5, and premature growthplate closure in 5. In the 8 cross-sectional gymnastics
studies reviewed, a distal physeal stress reaction was noted
on radiographs from 10% to 85% of the athletes. Although
the authors concluded that stress-related physeal injuries in
pediatric athletes often resolve without growth complication after adequate rest and rehabilitation,16 prospective,
randomized studies must be performed to provide stronger
evidence before clinicians should relax their vigilance
concerning the potential for growth disturbance.
An estimated 50% of overuse injuries in physically active
children and adolescents may be preventable.5 The
prevention of pediatric overuse injuries requires a comprehensive, multidimensional approach that includes (1)
improved injury surveillance (ie, improved understanding
of epidemiology), (2) identification of risk factors for
injury, (3) thorough PPEs, (4) proper supervision and
education (both coaching and medical), (5) sport alterations, (6) improved training and conditioning programs,
and (7) delayed specialization. This preventive approach
has been advocated by several prominent sports and health
care organizations, including the American College of
Sports Medicine,5 the World Health Organization and
International Federation of Sports Medicine,13 the American Academy of Pediatrics,31 and the International
Olympic Committee.12
Injury Surveillance
Before implementing any new prevention strategies or
aiming to improve injury management, we must have
adequate studies of epidemiology and a good understanding of the risk factors for pediatric overuse injuries.15 The
literature regarding the epidemiology of overuse injuries in
pediatric athletes is scarce at best, particularly the literature
concerning American children.
However, the epidemiology of chronic injuries has been
investigated in several international studies. In a 2003
Japanese study,46 the authors reviewed 196 stress fractures
(125 males, 71 females) among 10 726 patients over a 10year period. The average age of those with stress fractures
was 20.1 years (range, 10–46 years), with 42.6% of patients
between the ages of 15 and 19 years. The location of the
stress fracture was somewhat specific to sport: the
olecranon in baseball players, ribs in rowers, and tibial
shaft stress fractures in ballet dancers, runners, and tennis,
basketball, and volleyball players. Basketball players also
sustained stress fractures to the metatarsals, whereas track
athletes and soccer players incurred stress fractures to the
tibial shaft and pubic bone. The authors concluded that
stress fractures were common in high-functioning adolescent athletes, with similar proportions among male and
female athletes. In another Japanese study29 of stress
fractures in 208 athletes under the age of 20 years, the
researchers found that the peak age of occurrence was
16 years, the most frequent site was the tibial shaft, and
basketball was the sport most commonly associated with
stress fractures. A 2006 retrospective study47 of stress
fractures among 25 juveniles demonstrated that the age of
onset was 12.9 6 4.3 years (range, 3–17 years) and the tibia
was most often affected (48%, n 5 13), followed by the
metatarsals (18.5%, n 5 5). Using data from the High
School Report Injuries Online (RIO) injury surveillance
system, Fernandez et al48 reported that 4350 athletic
injuries occurred among athletes participating in 9 high
school sports during 1 academic year. Although these
authors did not focus solely on overuse injuries, they noted
that 53% (n 5 2298) of these injuries were to the lower
extremity; 2% of these injuries were classified as tendinitis
and 1.3% as stress fractures. Specific investigations of the
epidemiology of overuse injuries are warranted in the high
school population.
Although studies on the general prevalence of pediatric
overuse injuries are lacking, investigators have addressed
the sport-specific prevalence of overuse injuries. Dubravcic-Simunjak et al2 retrospectively surveyed 469 elite
junior figure skaters in Croatia, with 42% of female skaters
and 45% of male skaters self-reporting an overuse injury at
some point in their skating careers. In female singles ice
skaters, the most frequent injury was a stress fracture
(approximately 20%), followed by patellar tendinitis
(14.9%). Male singles ice skaters were more likely to
experience jumper’s knee (16%), followed by OsgoodSchlatter disease (14.2%). Maffulli et al49 reported on
overuse injuries of the elbow among elite gymnasts in the
United Kingdom and found that 12 elbows of 8 patients
(aged 11–15 years) displayed a spectrum of radiologic
abnormalities, including olecranon physis widening and
epiphyseal fragmentation.
In a recent investigation of Norwegian soccer players,
the rates of overuse injuries were 0.2 (95% confidence
interval [CI] 5 0.1, 0.4) and 0.4 (95% CI 5 0.0, 0.8) per
1000 player-hours in 6- to 12-year-old boys and girls,
respectively.50 An increase in the incidence of overuse
injuries was noted in an older cohort (13–16 years old) of
boys (0.7, 95% CI 5 0.4, 1.0) and girls (0.7, 95% CI 5 0.3,
1.1) per 1000 player-hours, with the relative risk (RR) of
overuse injury calculated as 2.9 (95% CI 5 1.3, 6.4) and 1.7
(95% CI 5 0.6, 5.5) in older boys and girls, respectively.50
In addition, 87% of the reported overuse injuries resulted
in time loss from soccer that ranged from 1 to more than
21 days. Similarly, LeGall et al51 investigated the incidence
of soccer-related injuries in elite French youth players and
found that those younger than age 14 had more injuries
during training sessions (ie, practices) and more growthrelated overuse injuries, whereas older athletes more often
sustained injuries during games. Overuse injuries accounted for 17.2% of all injuries and were mainly classified as
tendinopathies (n 5 108, 9.4%), osteochondroses (n 5 72,
Journal of Athletic Training
209
6.3%), or other overuse (n 5 19, 1.6%). In a follow-up
study of adolescent female soccer athletes over 8 seasons,
overuse injuries accounted for 13.4% of all injuries.52
We need to better understand the prevalence, incidence,
and economic impact of overuse injuries among pediatric
athletes in the United States. Although few data are
currently available about overuse injuries, the more than
7.5 million young people who participate in interscholastic
sports53 and millions of others who participate in youth
sports programs across the country represent a very large
at-risk population worthy of the expenditure of time,
effort, money, and improved surveillance by clinicians and
researchers alike.
Preparticipation Physical Examination
A consensus has emerged that the PPE, as defined by
several leading medical and allied health specialty societies,
is the primary means of identifying at-risk athletes and
initiating preventive measures.5,6,14,15,17 The main objectives of the PPE are to detect life-threatening or disabling
medical or musculoskeletal conditions and to screen
athletes for medical or musculoskeletal conditions that
may predispose them to injury or illness.17 In the context of
this position statement, the history and musculoskeletal
examination are important in detecting and possibly
preventing overuse injuries. Additional information on
other aspects of the PPE can be obtained from the
Preparticipation Physical Evaluation monograph.17
The history portion of the PPE should be used to
recognize previous injuries and other possible signs of
overtraining. Many overuse injuries can be identified from
the answers provided in the history component.17 Furthermore, a history of stress fractures or chronic or recurring
musculoskeletal injuries may be associated with nutritional
insufficiencies, which should be investigated as needed.17
The physical examination of the musculoskeletal system
should include evaluation of the athlete’s physical stature
and maturity (Tanner stage) and any deficits in strength
and flexibility.5,17 In addition, the stability, symmetry, and
range of motion of all joints and the relative symmetry,
strength, and flexibility of all major muscle groups should
be evaluated. These musculoskeletal assessments include
range-of-motion tests, manual muscle tests, joint stress
tests, flexibility tests, and balance tests, compared bilaterally. The Preparticipation Physical Evaluation17 describes
the general 14-point musculoskeletal screening examination as an acceptable approach to evaluate the musculoskeletal system in athletes who are asymptomatic and
without a history of previous injury. If the athlete describes
a previous injury in the history portion or pain or positive
findings are noted on the general screening examination, a
more thorough joint-specific examination should be
conducted.17 Ideally, a biomechanical assessment or
functional screening test(s) should be incorporated to
evaluate overall posture, gait mechanics, core stability,
and functional strength.54 This may include either a single
functional screening test, such as the overhead squat test,55
or a series of tasks56 to identify abnormal movement
patterns. However, these tasks have yet to be validated in
the pediatric population. Any deficits or concerns should
be discussed with the athlete and parent, along with
recommendations for correcting these deficits, including
210
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N Number 2 N April 2011
referral to a physician specialist, athletic trainer, or
physical therapist if needed.5,14,15 Future researchers
should focus on improving aspects of the musculoskeletal
history, validating the general 14-point musculoskeletal
screening examination and incorporating additional
screening tests as possible predictors of overuse injuries.
A well-designed PPE can serve as a screening process
from which prevention mechanisms can be developed.57
This process should be simple to administer and reliable
and should use a combination of anthropometric and
biomechanical measures to identify risk factors. Unfortunately, the PPE is often incompletely and inconsistently
delivered. In most states, the PPE is mandated for high
school athletes, but it is often not a requirement for those
participating in club-based or youth sports. Required
elements in the history and physical examination vary
widely and are often not consistent with published national
guidelines.58 The Preparticipation Physical Evaluation17
suggests that the ideal location for the PPE is within the
athlete’s primary care physician’s office; however, it
acknowledges other approaches, including the coordinated
medical team examination and, although not recommended, the locker room-based examination. As a
consequence of the lack of mandates, many adolescents
seek their PPEs with a variety of providers and may be
diverted from a medical ‘‘home,’’ where they can receive
ongoing health immunizations and screening for the
common psychosocial morbidities of adolescence.59 The
lack of continuity also precludes connection with the
rehabilitative follow-up deemed essential to injury prevention.60
Finally, the PPE may not be able to meet criteria for an
appropriate screening process, even if implemented perfectly, because it is neither sensitive nor specific enough to
adequately detect the life-threatening medical conditions
that are so exceedingly rare60 or, in its current state, predict
the potential for overuse injuries. Furthermore, as noted
throughout this position statement, the evidence base is
lacking as to which historical, anthropometric, and
biomechanical findings confer increased musculoskeletal
injury risk and which may be amenable to preventive
interventions.
Identification of Risk Factors
Little rigorous research has been conducted to investigate potential risk factors for overuse injuries in pediatric
athletes. Table 2 lists a number of suspected growth-related
intrinsic and extrinsic risk factors for overuse injuries,
although these classifications and listings of risk factors are
primarily based on anecdotal evidence.9,61
One group10 attempted to identify accident-prone and
overuse-prone profiles in young adults by prospectively
investigating the effects of numerous physical and psychosocial characteristics on the rate of acute and overuse
injuries. They developed an overuse-injury–prone profile
for both males and females, which included physical
factors such as a lack of stability (eg, decreased static
strength coupled with laxity), muscle tightness, malalignment, more explosive strength, and large body size (ie,
height and mass), and psychological traits including degree
of carefulness, dedication, vitality, and sociability (Table 3).10 Many of these characteristics (eg, anatomical
Table 2. Potential Risk Factors Predisposing Pediatric Athletes to Overuse Injuriesa
Growth-Related Factors
Intrinsic Factors
Extrinsic Factors
Cartilage at growth plate is more susceptible to injury
Period of adolescent growth increases the risk of injury
(eg, osteochondritis dissecans, apophysitis, physeal
injuries)
Previous injury
Malalignment
Menstrual cycle
Psychological issues
Muscle imbalances
Inflexibility
Muscle weakness
Instability
Level of play
Age
Height
Sex
Tanner stage
Laxity
Experience
Training and recovery
Equipment
Poor technique
Psychological issues
Training errors
Environment
Sport-acquired deficiencies
Conditioning
a
From DiFiori9 and O’Connor et al.61
alignment, flexibility, strength, speed) can be measured
during a PPE or baseline fitness test, allowing clinicians to
identify athletes potentially at risk for overuse injuries and
to develop preventive measures.
Not surprisingly, baseball has been the most widely
studied youth sport in the United States. Lyman et al18
prospectively evaluated 9- to 12-year-old baseball pitchers
for pain or soreness in the shoulder or elbow during or
after a pitching outing. Over 2 seasons, shoulder or elbow
pain was noted in 47% (n 5 141) of the pitchers, with most
of the pain complaints considered mild (ie, without loss of
time in games or practices). The authors also provided
some associated pain-related factors that may be important
in identifying those potentially at risk for subsequent
overuse injuries. Elbow pain was related to increased age,
decreased height, increased mass, increased cumulative
pitch counts, arm fatigue, decreased self-perceived performance, participation in a concurrent weightlifting program, and participation in additional baseball leagues.18
The presence of shoulder pain was associated with an
increased number of pitches thrown in games, increased
cumulative pitch counts, participating with arm fatigue,
and decreased self-perceived performance. Both arm
fatigue and self-perceived performance were risk factors
for both elbow and shoulder pain. Therefore, pain should
not be ignored, because it is often the first indicator of an
overuse problem.20 Rest should be incorporated in all
programs; athletes who participated with arm fatigue were
Table 3. Profiles of Overuse-Injury–Prone Male and Female
Young Athletesa
Males
Females
Tall stature
Endomorph body structure
Less static strength
More explosive strength
Decreased muscle flexibility
High degree of ligamentous laxity
Large Q angle
Tall stature
Decreased upper extremity strength
Less static strength
More explosive strength
High limb speed
Increased muscle tightness
Increased ligamentous laxity
Greater leg-length discrepancy
Pronation
Large Q angle
a
From Lysens et al.10
almost 6 times more likely to suffer from elbow pain and 4
times more likely to have shoulder pain that those who did
not have arm fatigue.18
A subsequent investigation20 of 3 suspected risk factors
(pitch type, pitch count, and pitching mechanics) found
that the use of breaking pitches and high pitch counts
increased the risk of both elbow and shoulder pain among
youth pitchers. Specifically, the risk of elbow pain among
pitchers using the slider increased 86% and the risk of
shoulder pain in those throwing curveballs increased 52%.
In addition, higher single-game pitch counts and higher
cumulative (season-long) game pitch counts were associated with an increased risk of shoulder pain. This association
between game pitch count and shoulder injury was
strongest among 9- to 10-year-old and 13- to 14-year-old
pitchers. Interestingly, pitching mechanics were not significantly associated with either elbow or shoulder pain in any
of the age groups studied.20 The authors20 concluded that
changeups remain the safest pitch for 9- to 14-year-olds to
throw and that pitch limits, rather than inning limits, may
be a better indicator of when pitchers should be removed
from pitching to allow adequate rest.
More recently, Olsen et al19 investigated risk factors for
shoulder and elbow injuries in adolescent pitchers. Group
analyses between pitchers with or without elbow or
shoulder injury revealed that a greater percentage of
injured pitchers started at another position before pitching,
pitched with arm fatigue, and continued to pitch even with
arm pain.19 In addition, those who suffered an injury had a
greater fastball speed and participated in a greater number
of showcases (multiday, high-level events in which athletes
may participate in numerous games within a short time
span). A subsequent factor analysis revealed the following
risk factors: participating in more than 8 months of
competitive pitching (odds ratio [OR] 5 5.05, 95% CI 5
1.39, 18.32), throwing more than 80 pitches per appearance
(OR 5 3.83, 95% CI 5 1.36, 10.77), having a fastball speed
greater than 85 mph (136.8 kph) (OR 5 2.58, 95% CI 5
0.94, 7.02), and pitching either infrequently (OR 5 4.04,
95% CI 5 0.97, 16.74) or regularly (OR 5 36.18, 95% CI 5
5.92, 221.22) with arm fatigue.19
With respect to lower extremity injuries, few authors
have attempted to identify specific overuse-injury risk
factors in pediatric athletes, and their findings are
Journal of Athletic Training
211
inconclusive. These studies are limited to research on
medial tibial stress syndrome (MTSS) and stress fractures.30,62,63 In 2 investigations of risk factors for MTSS in
high school cross-country runners, predictive variables
differed.62,63 One group62 found that athletes with MTSS
had a greater navicular drop (6.6 mm) than those who were
asymptomatic (3.6 mm) and that the combination of
navicular drop and sex accurately predicted 78% of MTSS
cases. However, resting calcaneal position, tibiofemoral
varum, and gastrocnemius length (ie, tightness) were not
predictive. A subsequent investigation63 revealed that sex
and body mass index were predictors of MTSS, with the
latter being the only predictor when controlling for
orthotic use. Additionally, compared with those without
an injury history, high school cross-country runners with a
history of previous injury were 2 times more likely to report
MTSS (OR 5 2.18, 95% CI 5 0.07, 6.4) and 3 times more
likely to use orthotics (OR 5 3.0, 95% CI 5 0.09, 9.4).63
Correlates of stress fractures in a general population of
female adolescents have also been researched and, although
age had the strongest association with a stress-fracture
history (27% to 29% increased odds for each year beyond
age 11), participation in more than 16 hours per week of
vigorous activity (OR 5 1.88, 95% CI 5 1.18, 3.03) and in
high-impact physical activity, such as basketball, soccer,
volleyball, running, tennis, or cheerleading (OR 5 1.06,
95% CI 5 1.03, 1.10), was also related to stress-fracture
history.30 They reported a slight (but nonsignificant)
increased risk for stress fracture in the most sedentary
girls, a reminder that participation in impact-loading
physical activity is important in this population because
of its positive effects on bone mineral density.30
In a subsequent clinic-based study of adolescent female
athletes, only family history of osteoporosis or osteopenia
was associated with stress fracture (OR 5 2.96, 95% CI 5
1.36, 6.45).64 However, in neither adolescent athlete
investigation was stress fracture associated with irregular
menstrual periods, as has been demonstrated in adult
women athletes and military recruits.65 In combination,
these investigations may begin to identify safe thresholds
for participation in vigorous physical activity (16–20 h/wk).
They also suggest that risk stratification must incorporate
both intrinsic (eg, inherited skeletal quality) and extrinsic
(eg, training volume) factors. Another area of focus
concerning risk factors has been generalized joint hypermobility, which is characterized by mobility of multiple
joints beyond the normal range of motion. Community
prevalence of generalized joint hypermobility appears to
depend on age, sex, and race, with reports ranging from 2%
(adult Caucasian males) to 57% (African females of mixed
ages).66 A considerable number of studies of rheumatology
and pediatric clinic-based populations appear to demonstrate relationships between generalized joint hypermobility and insidious-onset arthralgia and fibromyalgia.67–75
Yet prospective studies of nonclinic populations are at best
inconclusive as to whether joint hypermobility increases
injury risk.
In a prospective study23 of 17-year-old military recruits,
those with hypermobility had more injuries during boot
camp than those who were not hypermobile. Another
prospective study24 of youngsters 6 to 14 years old
demonstrated that children with hypermobile joints had
more complaints of joint pain than nonhypermobile
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Volume 46
N Number 2 N April 2011
children. A retrospective study76 of pediatric (aged 6–
16 years) netball players in Australia showed that
hypermobility was associated with an increased prevalence
of self-reported injuries. In another small retrospective
study77 including children and adults, more injuries were
reported by hypermobile ballet dancers than by their
nonhypermobile counterparts. In an attempt to describe
overuse-prone profiles of young adults, Lysens et al10
reported that males and females with weak muscles, poor
flexibility, and hypermobility may be at increased risk for
overuse injuries.
Alternately, several prospective studies of mixed (child
and adult) or adult athletic populations do not support the
conclusion that joint hypermobility is related to injury risk.
A prospective study78 of netball players aged 15 to 36 years
demonstrated no differences in injuries based on hypermobility status. Studies of National Collegiate Athletic
Association lacrosse players79 and professional soccer
players80 also have indicated no differences in injuries
based on hypermobility status. Finally, a retrospective
study81 of female gymnasts aged 10 to 21 years found no
relationship between hypermobility status and reported
history of injuries.
Screening for generalized joint hypermobility is relatively
easy using the methods first proposed by Carter and
Wilkinson82 and later modified by Beighton and Horan.83
This multijoint active range-of-motion screening procedure
is widely accepted (Table 4). Incorporating this screening
into the PPE might add only a few minutes to each
assessment, but its use should depend upon the time, cost,
and level of experience of the examiner administering the
PPE.
Proper Supervision and Education
Organizations sponsoring interscholastic or club-based
athletics in which pediatric athletes participate have the
responsibility to ensure adequate coaching and medical
supervision.5,13,14 Proper supervision by coaches and
enforcement of the rules of the sport (which includes
adequate education of both coaches and officials) may
serve as a means to decrease overuse injury risk in this age
group.9,15,50 For example, Little League Baseball provides
pitch-count regulation (Appendix A), tracking sheet
(Appendix B), and pitching eligibility forms, all of which
are easily accessible to youth baseball coaches. The
guidelines mandating pitch-count limits are adapted from
scientific evidence and are updated frequently as new
research emerges.84 Moreover, proper medical supervision
at competitions and practices may allow for early
recognition of overuse injuries in the beginning stages to
permit proper evaluation, referral, and rehabilitation
before they result in time lost from participation.14,15
Education of all athletes, parents, coaches, and officials
regarding overuse injuries and preventive mechanisms is
advocated. Athletes, parents, and coaches should all have
knowledge of general signs and symptoms of overuse,
including but not limited to a gradual onset of pain, pain
presenting as an ache, no history of direct injury, stiffness
or aching after or during training or competition,
increasing periods of time for pain to resolve, point
tenderness, visible swelling, missed training sessions as a
result of the pain or injury, and a problem that persists.25
Table 4. The Beighton and Horan Joint Mobility Indexa
Test
Wrist flexion, thumb
opposition
Fifth metacarpal extension
Elbow extension
Trunk and hip flexion
Knee extension
a
b
Description
Scoringb
Stabilize the distal portion of the forearm. The thumb being
tested is passively abducted by the fingers of the opposite
hand toward the volar aspect of the forearm with the wrist
in flexion.
The patient sits with the arm in 806 of abduction and the
elbow flexed to 906. The forearm rests on the table in
a pronated position. The fifth metacarpal is extended.
The patient sits with the shoulder flexed to 906 and the
forearm supinated.
The patient stands and then flexes at the waist, attempting
to touch the palms flat to the floor while keeping the
knees either extended or hyperextended.
The patient lies supine with 1–2 towels placed under the
ankles.
Score 1 point for each thumb that can be passively
bent to touch the forearm.
Score 1 point for each metacarpal that extends
past 906.
Score 1 point for each elbow that can actively
hyperextend past 06.
Score 1 point if the patient can bend at the waist
and place the hands flat on the floor without
bending the knees.
Score 1 point for each knee that can passively
hyperextend past 06.
From Carter and Wilkinson82 and Beighton and Horan.83
Total possible points 5 9.
These signs and symptoms should not be ignored as
‘‘growing pains’’ but should be taken seriously by the
athlete, parent, and coach. Athletes involved in runningbased sports should be educated regarding sensible training
habits and the proper fit and selection of running shoes to
reduce impact forces. Athletes involved in throwing sports
should be educated as to the potential risk factors for
upper extremity overuse injuries, with specific emphasis on
using arm fatigue as an indicator to stop throwing.18,19 All
athletes should be educated on proper exercise progression
and should gradually increase time, distance, and intensity
by the 10% rule (see ‘‘Training and Conditioning’’ section
below).57
To our knowledge, no published studies have addressed
the general knowledge of overuse injuries among coaches;
however, reports describe the general lack of first aid,
injury recognition, and management knowledge of high
school26 and youth27 coaches. No mandated national
coaching education program exists in the United States
for youth sports, and the requirements for high school
athletic coaches vary from state to state, with some
requiring only first aid and cardiopulmonary resuscitation
(CPR) certification. However, numerous coaching education programs provide information related to proper
biomechanics of sporting skills, nutrition, physical conditioning, development of athletes, and prevention, recognition, and management of injuries (Table 5). Completion
of at least 1 of these courses is recommended for all
coaches working with pediatric athletes. Additionally,
coaches should be encouraged to maintain their certifications and participate in continuing education opportunities to remain current with the latest sports safety
information.
Sport Alterations
Alterations or modifications to the existing rules for
adults may prevent overuse injuries in children and
adolescents.5,13,31 These modifications may be simple,
including shorter quarters or halves, bases closer together,
Table 5. Coaching Education Programs
Organization
Training Focus
National Athletic Trainers’
Association Sports Safety for
Youth Coaches
National Youth Sports Coaches
Association
American Sports Education
Program
Recognition of illnesses and injuries, safe playing
conditions, training and conditioning, emergency
planning
General youth sports
Sport-specific training
Technical and tactical skills of sport
Cardiopulmonary resuscitation, automated external
defibrillator certification, coaching essentials, and
sports first aid courses
Sports safety that teaches participants to recognize
and prevent common athletic injuries, emergency
preparedness, first aid management, and sport
enjoyment
Environmental hazards, emergency situations, and
decision making for first aid care
‘‘Fundamentals of Coaching’’ course
National Center for Sports
Safety (PREPARE)
American Red Cross
National Federation of State
High School Associations
Online first aid course
Format
Web Address
Online
http://www.nata.org
Online
Online
https://www.nays.org/onlinepromo/
OnlineHome.html
http://www.asep.com/
Online
http://www.sportssafety.org/prepare/
Classroom
http://www.redcross.org/services/
hss/courses/sports.html
http://www.nfhslearn.com/
CourseDetail.aspx?
courseID51000
http://www.nfhslearn.com/
CourseDetail.aspx?
courseID51001
Online
Journal of Athletic Training
213
Table 6. Recommendations for Pitch Counts on the First 4 Days After a Pitching Eventa
Pitch Count
Age, y
1 d Rest
2 d Rest
3 d Rest
4 d Rest
9–10
11–12
13–14
15–16
17–18
21–33
27–34
30–35
30–39
30–39
34–42
35–54
36–55
40–59
40–59
43–50
55–57
56–69
60–79
60–89
51+
58+
70+
80+
90+
a
From Andrews and Fleisig.21 Reprinted with permission from USA Baseball.
less frequent games or practices, or pitch-count limits; or
they may be more complex, such as the recommendation to
match athletes by height, maturity, or skill as opposed to
age.
Some experts are now moving away from the long-held
and perhaps largely anecdotal belief that throwing
breaking pitches is related to arm injuries in young baseball
players. The only prospective study20 we were able to find
appears to support this belief: pitchers throwing sliders had
an 86% increased risk of elbow pain, and pitchers throwing
curveballs had a 52% increased risk of shoulder pain.
However, biomechanical studies comparing torque and
moments generated by different types of pitches in 11- to
14-year-olds85 and 14- to 18-year-olds86 showed that the
fastball imposed more demand than the curveball. Based
on the results of these biomechanics studies, some
researchers have postulated that throwing breaking pitches
is not necessarily risky for young athletes. Yet it is
important to recognize that the participants in these studies
were healthy, with no history of arm injury, and, in the case
of the Nissen et al86 study, perhaps slightly older than the
players who are generally the target of the recommendation
against throwing breaking balls.
Furthermore, pitching limits should be established for 9to 14-year-olds, with full-effort (ie, competition) throwing
limited to 75 pitches per game and 600 pitches per season.20
Young throwers should also have adequate rest after a
pitching event and adjust pitch limits for those rest days
Table 7. Suggested Sport-Modification Recommendations for
Adolescent Pitchersa
1. Avoid pitching with arm fatigue.
2. Avoid pitching with arm pain.
3. Avoid pitching too much. Future research needed, but the following
general limits are
a. Avoid pitching more than 80 pitches per game.
b. Avoid competitive pitching more than 8 months of the year.
c. Avoid pitching more than 2500 pitches in competition per year.
4. Pitchers with the following characteristics should be monitored closely
for injury
a.
b.
c.
d.
e.
f.
a
Those who regularly use anti-inflammatories to ‘‘prevent’’ injuries
Regularly starting pitchers
Pitchers who throw . 85 mph (137 kph)
Taller and heavier pitchers
Pitchers who warm up excessively
Pitchers who participate in showcases
Olsen SJ II, Fleisig GS, Dun S, Loftice J, Andrews JR, American
Journal of Sports Medicine, 905–912, copyright g2006 by SAGE
Publications. Reprinted by permission of SAGE Publications.
214
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accordingly (Table 6). Table 7 lists baseball-pitcher–specific modification recommendations.
In addition to Little League, other athletic governing
bodies and organizations have instituted sport modifications. The US Cycling Federation has imposed gear-ratio
limits for athletes between 10 and 16 years of age,54 limiting
the maximal stress or effort in those at the lower end of
that age range. Running organizations in Australia also
have age-related regulations, including set distances in
which younger athletes may participate. Adolescents can
begin participating in 5-km (3.1-mile) races at age 12 and in
10-km (6.2-mile) races at age 14. Half-marathon (21.1-km;
13.1-mile) and marathon (42.2-km; 26.2-mile) distances can
be run beginning at ages 15 to 16 and .18 years,
respectively.54 As described in Table 8, USA Swimming
has recommendations for the number of sessions per week
and the length of each session for various levels of
competitive age-group swimming.87
Training and Conditioning
Proper training and conditioning, both before and during
the season, may prevent overuse injuries. Unfortunately, in
today’s society, many youngsters are not as active as
previous generations, leading to a phenomenon of cultural
deconditioning.88,89 There has been a general decline in
physical activity, including free play, walking to school, and
regular physical-education classes, with a concurrent increase in sedentary activities, including watching television,
playing video games, and, in some cases, physical activity
limited to sport participation. Athletes with poorer levels of
general fitness or conditioning may not be able to tolerate
the demands of training required for sport participation.
Therefore, all pediatric athletes should begin by establishing
a good general-fitness routine that encompasses strengthening, endurance, and flexibility.5,9,37 Sufficient participation in general strength, endurance, and flexibility training,
as well as lifestyle physical fitness (eg, taking the stairs
instead of the elevator), should precede sport-specific
training.38 Once a general foundation of fitness has been
established, athletes should begin to gradually increase their
training loads. Pediatric athletes are advised to follow the
10% rule, which allows for no more than a 10% increase in
the amount of training time, distance, repetitions, or load
each week.5,31 For example, a runner who is currently
running 15 miles/wk (24 km/wk) should only be allowed to
increase mileage to 16.5 miles (27 km) the following week.
Similarly, athletes participating in strength training should
increase only either repetitions or weight by 10% each week,
not both. The goal of the 10% rule is to allow the body to
adjust gradually to increased training intensity.
Table 8. Developmental Progression for Pediatric Swimmersa
Level
Category
1
Sport preparation: ages 6–9 y
2
Basic skill development: ages 8–11 y
3
Basic training development: ages 11–14 y
4
Progressive training: ages 13–18 y
5
Advanced training: age 14 y and older
a
Commitment
2–3 sessions/wk
30–60 min/session
2–4 sessions/wk
30–60 min/session
Encourage other activities, sports
Intrasquad or low-pressure competition
4–6 sessions/wk
60–90 min/session
Year-round participation
Encourage other activities, sports while understanding the need to meet
attendance expectations
6–10 sessions/wk
90–120 min/session
Year-round competition
Including long-course (50-m pool-length) competition
Commit to swimming
Shorter breaks to minimize deterioration of aerobic base
8–10 sessions/wk
90–120 min/session
Year-round
High commitment level
Short breaks to minimize deterioration of aerobic base
Reprinted with permission from USA Swimming.87
More recently, preventive training programs have been
targeted specifically at the pediatric athlete. Although the
primary focus of many of these programs has often been
for the prevention of noncontact anterior cruciate ligament
injuries, several authors34–36 have also investigated whether
overuse-injury risk could be reduced among program
participants. In a prospective study of a structured warmup program including technique training, neuromuscular
control, and balance and strengthening exercises, Olsen et
al36 reported that participants had a reduction in overall
injuries (RR 5 0.49, 95% CI 5 0.36, 0.68), lower limb
injuries (RR 5 0.51, 95% CI 5 0.36, 0.74), and overuse
injuries (RR 5 0.43, 95% CI 5 0.25, 0.75). Similarly, a
program that focused on educating and training coaches to
incorporate an overall-prevention mentality (consisting of
improved warm-up, cool-down, taping unstable ankles,
rehabilitation, promoting fair play, and a set of 10 exercises
designed to improve joint stability, flexibility, strength,
coordination, reaction time, and endurance) resulted in a
reduction in both total injuries (0.76 6 0.89 versus 1.18 6
1.04, P , .01) and overuse injuries (0.26 6 0.48 versus 0.44
6 0.65, P , .05) per player-year.35 Specific to physically
active adolescents, a 6-month, home-based balance-training program resulted in improvements in both static and
dynamic balance among program participants.34 However,
because of the limited number of injuries reported, no
conclusions regarding the effectiveness of the program on
reducing injuries could be drawn. Still, a clinically
important difference was noted in self-reported injuries:
program participants reported 3 (95% CI 5 5, 35) injuries
per 100 adolescents, compared with 17 (95% CI 5 3, 24) in
the control groups. Interestingly, the program was more
effective in reducing injuries among those adolescents who
reported sustaining an injury in the previous year,90 thus
highlighting the need to identify injury history through a
thorough PPE. In general, programs that are successful in
reducing the risk of overuse injuries among pediatric
athletes seem to include strengthening, neuromuscular
control, flexibility exercises, balance, and technique training.
Delayed Specialization
One of the more controversial areas with respect to
pediatric overuse injuries deals with the early specialization
of athletes participating in the same sport year-round from
a young age. Although little evidence-based research
demonstrates that this practice has negative consequences
on physical growth or psychological outcomes, many
clinicians and health care organizations have advocated
for diversity in sport participation or delayed specialization.5,9,91,92,93 It is theorized that participation in only 1
sport can result in increased risk for repetitive microtrauma
and overuse5 or that multisport athletes who do not obtain
adequate rest between daily activities or between seasons
and those who participate in 2 or more sports that
emphasize the same body part are at higher risk for
overuse injuries than those in multiple sports with different
emphases.31
Young athletes who participate in a variety of sports
tend to have fewer injuries and play longer, thereby
maintaining a higher level of physical activity than those
who specialize before puberty.92 In addition to the
potential for repetitive microtrauma and overuse injury,
specialization in 1 sport may be associated with nutritional
and sleep inadequacies, psychological or socialization
issues, and ultimately burnout. These problems might be
avoided with a balanced lifestyle and a strong support
system made up of parents, friends, coaches, and health
care providers.12
CONCLUSIONS
The major objective in managing repetitive or training
injuries in athletes of any age should be to determine risk
factors for injury and identify steps to prevent the
occurrence of these injuries. Knowledge is growing about
Journal of Athletic Training
215
risk factors for the occurrence of both acute traumatic
injuries and repetitive microtrauma overuse injuries in
adults, particularly in such activities as military training,
work activities, and sports. However, too little is known
about risk factors for overuse injury in pediatric athletes.
Injury surveillance in young athletes should be improved
to record the occurrence of injury and the determination of
associated risk factors, as well as epidemiologic data (eg,
age, sex, height, mass, and, if possible, Tanner stage).
Epidemiologic studies in specific environments in pediatric
populations would add greatly to the understanding of the
risk associated with particular sport activities, thus
providing a foundation for future studies of prevention
and treatment efficacy.
ACKNOWLEDGMENTS
We gratefully acknowledge the efforts of Michael C. Koester,
MD, ATC; Laura Purcell, MD; Angela Smith, MD; and the
Pronouncements Committee in the preparation of this document.
DISCLAIMER
The NATA publishes its position statements as a service to
promote the awareness of certain issues to its members. The
information contained in the position statement is neither
exhaustive not exclusive to all circumstances or individuals.
Variables such as institutional human resource guidelines, state or
federal statutes, rules, or regulations, as well as regional
environmental conditions, may impact the relevance and implementation of these recommendations. The NATA advises its
members and others to carefully and independently consider each
of the recommendations (including the applicability of same to
any particular circumstance or individual). The position statement should not be relied upon as an independent basis for care
but rather as a resource available to NATA members or others.
Moreover, no opinion is expressed herein regarding the quality of
care that adheres to or differs from NATA’s position statements.
The NATA reserves the right to rescind or modify its position
statements at any time.
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Address correspondence to Tamara C. Valovich McLeod, PhD, ATC, Athletic Training Program, A.T. Still University, 5850 E. Still
Circle, Mesa, AZ 85206. Address e-mail to tmcleod@atsu.edu.
218
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Journal of Athletic Training
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Appendix A. Little League Pitch Count Tracker. Form provided by Little League International, Williamsport, PA.
220
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Appendix B. Little League Pitcher Eligibility Tracker. Form provided by Little League International, Williamsport, PA.
Official Statement from the National Athletic Trainers’ Association
on Communicable and Infectious Diseases in Secondary School Sports
The National Athletic Trainers’ Association (NATA) recommends that health care professionals
and participants in secondary school athletics take the proper precautions to prevent the spread
of communicable and infectious diseases.
Due to the nature of competitive sports at the high school level, there is increased risk for the
spread of infectious diseases, such as impetigo, community acquired methicillin-resistant
staphylococcus infection (MRSA) and herpes gladiatorum (a form of herpes virus that causes
lesions on the head, neck and shoulders). These diseases are spread by skin-to-skin contact and
infected equipment shared by athletes, generally causing lesions of the skin. The following
The following are suggestions from NATA to prevent the spread of infectious and communicable
diseases:
• Immediately shower after practice or competition
• Wash all athletic clothing worn during practice or competition daily
• Clean and disinfect gym bags and/or travel bags if the athlete is carrying dirty workout
gear home to be washed and then bringing clean gear back to school in the same bag.
This problem can also be prevented by using disposable bags for practice laundry.
• Wash athletic gear (such as knee or elbow pads) periodically and hang to dry
• Clean and disinfect protective equipment such as helmets, shoulder pads, catcher’s
equipment and hockey goalie equipment on a regular basis
• Do not share towels or personal hygiene products with others
• All skin lesions should be covered before practice or competition to prevent risk of
infection to the wound and transmission of illness to other participants. Only skin
infections that have been properly diagnosed and treated may be covered to allow
participation of any kind
• All new skin lesions occurring during practice or competition should be properly
diagnosed and treated immediately.
• Playing fields should be inspected regularly for animal droppings that could cause
bacterial infections of cuts or abrasions
• Athletic lockers should be sanitized between seasons
• Rather than carpeting, locker or dressing rooms should have tile floors that may be
cleaned and sanitized
• Weight room equipment, including benches, bars and handles should be cleaned and
sanitized daily
National Athletic Trainers’ Association
3-07
Journal of Athletic Training 2011:47(1):1–24
© by the National Athletic Trainers’ Association, Inc
www.nata.org/jat
position statement
National Athletic Trainers’ Association Position
Statement: Preventing Sudden Death in Sports
Douglas J. Casa, PhD, ATC, FNATA, FACSM* (co-chair); Kevin M.
Guskiewicz, PhD, ATC, FNATA, FACSM† (co-chair); Scott A.
Anderson, ATC‡; Ronald W. Courson, ATC, PT, NREMT-I, CSCS§;
Jonathan F. Heck, MS, ATC||; Carolyn C. Jimenez, PhD, ATC¶;
Brendon P. McDermott, PhD, ATC#; Michael G. Miller, PhD, EdD,
ATC, CSCS**; Rebecca L. Stearns, MA, ATC*; Erik E. Swartz, PhD,
ATC, FNATA††; Katie M. Walsh, EdD, ATC‡‡
*Korey Stringer Institute, University of Connecticut, Storrs; †Matthew Gfeller Sport-Related Traumatic
Brain Injury Research Center, University of North Carolina at Chapel Hill; ‡University of Oklahoma,
Norman; §University of Georgia, Athens; ||Richard Stockton College, Pomona, NJ; ¶West Chester
University, PA; #University of Tennessee at Chattanooga; **Western Michigan University, Kalamazoo;
††University of New Hampshire, Durham; ‡‡East Carolina University, Greenville, NC
In
Pr
udden death in sports and physical activity has a variety of causes. The 10 conditions covered in this position
statement are
• Asthma
• Catastrophic brain injuries
• Cervical spine injuries
• Diabetes
• Exertional heat stroke
• Exertional hyponatremia
• Exertional sickling
• Head-down contact in football
• Lightning
• Sudden cardiac arrest
(Order does not indicate rate of occurrence.)
Recognizing the many reasons for sudden death allows us to
create and implement emergency action plans (EAPs) that provide detailed guidelines for prevention, recognition, treatment,
and return to play (RTP). Unlike collegiate and professional
teams, which usually have athletic trainers (ATs) available,
nearly half of high schools as well as numerous other athletic
settings lack the appropriate medical personnel to put these
guidelines into practice and instead rely on the athletic director,
team coach, or strength and conditioning specialist to do so.
To provide appropriate care for athletes, one must be familiar with a large number of illnesses and conditions in order to
s
S
Recommendations: These guidelines are intended to provide relevant information on preventing sudden death in sports
and to give specific recommendations for certified athletic
trainers and others participating in athletic health care.
Key Words: asthma, cardiac conditions, diabetes, exertional
heat stroke, exertional hyponatremia, exertional sickling, head
injuries, neck injuries, lightning safety
es
Objective: To present recommendations for the prevention
and screening, recognition, and treatment of the most common
conditions resulting in sudden death in organized sports.
Background: Cardiac conditions, head injuries, neck injuries, exertional heat stroke, exertional sickling, asthma, and
other factors (eg, lightning, diabetes) are the most common
causes of death in athletes.
properly guide the athlete, determine when emergency treatment
is needed, and distinguish among similar signs and symptoms
that may reflect a variety of potentially fatal circumstances.
For the patient to have the best possible outcome, correct and
prompt emergency care is critical; delaying care until the ambulance arrives may result in permanent disability or death.
Therefore, we urgently advocate training coaches in first aid,
cardiopulmonary resuscitation (CPR), and automated external
defibrillator (AED) use, so that they can provide treatment until
a medical professional arrives; however, such training is inadequate for the successful and complete care of the conditions
described in this position statement. Saving the life of a young
athlete should not be a coach’s responsibility or liability.
For this reason, we also urge every high school to have an
AT available to promptly take charge of a medical emergency.
As licensed medical professionals, ATs receive thorough training in preventing, recognizing, and treating critical situations in
the physically active. Each AT works closely with a physician
to create and apply appropriate EAPs and RTP guidelines.
Throughout this position statement, each recommendation is labeled with a specific level of evidence based on the
Strength of Recommendation Taxonomy (SORT).1 This taxonomy takes into account the quality, quantity, and consistency
of the evidence in support of each recommendation: Category
A represents consistent good-quality evidence, B represents
Journal of Athletic Training
1
triggers, recognition of signs and symptoms, and compliance with monitoring the condition and taking medication as prescribed. Evidence Category: C
Recognition
4. The sports medicine staff should be aware of the major
asthma signs and symptoms (ie, confusion, sweating,
drowsiness, forced expiratory volume in the first second
[FEV1] of less than 40%, low level of oxygen saturation, use of accessory muscles for breathing, wheezing,
cyanosis, coughing, hypotension, bradycardia or tachycardia, mental status changes, loss of consciousness,
inability to lie supine, inability to speak coherently, or
agitation) and other conditions (eg, vocal cord dysfunction, allergies, smoking) that can cause exacerbations.4,5
Evidence Category: A
5. Spirometry tests at rest and with exercise and a field test
(in the sport-specific environment) should be conducted
on athletes suspected of having asthma to help diagnose
the condition.2,6 Evidence Category: B
6. An increase of 12% or more in the FEV1 after administration of an inhaled bronchodilator also indicates reversible airway disease and may be used as a diagnostic
criterion for asthma.7
Treatment
s
7. For an acute asthmatic exacerbation, the athlete should
use a short-acting β2-agonist to relieve symptoms. In a
severe exacerbation, rapid sequential administrations
of a β2-agonist may be needed. If 3 administrations of
medication do not relieve distress, the athlete should be
referred promptly to an appropriate health care facility.8
Evidence Category: A
8. Inhaled corticosteroids or leukotriene inhibitors can be
used for asthma prophylaxis and control. A long-acting
β2-agonist can be combined with other medications to
help control asthma.9 Evidence Category: B
9. Supplemental oxygen should be offered to improve the
athlete’s available oxygenation during asthma attacks.10
Evidence Category: B
10.Lung function should be monitored with a peak flow
meter. Values should be compared with baseline lung
volume values and should be at least 80% of predicted
values before the athlete may participate in activities.11
Evidence Category: B
11.If feasible, the athlete should be removed from an environment with factors (eg, smoke, allergens) that may
have caused the asthma attack. Evidence Category: C
12.In the athlete with asthma, physical activity should be
initiated at low aerobic levels and exercise intensity
gradually increased while monitoring occurs for recurrent asthma symptoms. Evidence Category: C
ASTHMA
Recommendations
In
Pr
es
inconsistent or limited-quality or limited-quantity evidence,
and C represents recommendations based on consensus, usual
practice, opinion, or case series.
The following rules apply to every EAP:
1. Every organization that sponsors athletic activities should
have a written, structured EAP. Evidence Category: B
2. The EAP should be developed and coordinated with local EMS staff, school public safety officials, onsite first
responders, school medical staff, and school administrators. Evidence Category: B
3. The EAP should be specific to each athletic venue. Evidence Category: B
4. The EAP should be practiced at least annually with all
those who may be involved. Evidence Category: B
Those responsible for arranging organized sport activities
must generate an EAP to directly focus on these items:
1. Instruction, preparation, and expectations of the athletes,
parents or guardians, sport coaches, strength and conditioning coaches, and athletic directors.
2. Health care professionals who will provide medical care
during practices and games and supervise the execution
of the EAP with respect to medical care.
3. Precise prevention, recognition, treatment, and RTP policies for the common causes of sudden death in athletes.
The EAP should be coordinated and supervised by the onsite AT. A sports organization that does not have a medical supervisor, such as an AT, present at practices and games and as
part of the medical infrastructure runs the risk of legal liability.
Athletes participating in an organized sport have a reasonable
expectation of receiving appropriate emergency care, and the
standards for EAP development have also become more consistent and rigorous at the youth level. Therefore, the absence
of such safeguards may render the organization sponsoring the
sporting event legally liable.
The purpose of this position statement is to provide an overview of the critical information for each condition (prevention, recognition, treatment, and RTP) and indicate how this
information should dictate the basic policies and procedures
regarding the most common causes of sudden death in sports.
Our ultimate goal is to guide the development of policies and
procedures that can minimize the occurrence of catastrophic
incidents in athletes. All current position statements of the National Athletic Trainers’ Association (NATA) are listed in the
Appendix.
Prevention and Screening
1. Athletes who may have or are suspected of having
asthma should undergo a thorough medical history and
physical examination.2 Evidence Category: B
2. Athletes with asthma should participate in a structured
warmup protocol before exercise or sport activity to decrease reliance on medications and minimize asthmatic
symptoms and exacerbations.3 Evidence Category: B
3. The sports medicine staff should educate athletes with
asthma about the use of asthma medications as prophylaxis before exercise, spirometry devices, asthma
2
Volume 47 • Number 1 • February 2012
Background and Literature Review
Definition, Epidemiology, and Pathophysiology. In 2009,
asthma was thought to affect approximately 22 million people
in the United States, including approximately 6 million children.4 Asthma is a disease in which the airways become inflamed and airflow is restricted.4 Airway inflammation, which
s
es
Pr
Figure 1. Asthma pharmacologic management. Abbreviations: CPR, cardiopulmonary resuscitation; PEF, peak expiratory flow; SABA,
short-acting β2-agonist. Casa DJ, Preventing Sudden Death in Sport and Physical Activity, 2012: Jones & Bartlett Learning, Sudbury, MA.
www.jblearning.com. Reprinted with permission.
In
may lead to airway hyperresponsiveness and narrowing, is associated with mast cell production and activation and increased
number of eosinophils and other inflammatory cells.2,3 Cellular
and mediator events cause inflammation, bronchial constriction
via smooth muscle contraction, and acute swelling from fluid
shifts. Chronic airway inflammation may cause remodeling and
thickening of the bronchiolar walls.12,13
Clinical signs of asthma include confusion, sweating,
drowsiness, use of accessory muscles for breathing, wheezing,
coughing, chest tightness, and shortness of breath. Asthma may
be present during specific times of the year, vary with the type
of environment, occur during or after exercise, and be triggered
by respiratory infections, allergens, pollutants, aspirin, nonsteroidal anti-inflammatory drugs, inhaled irritants, exposure to
cold, and exercise.5
Prevention. Athletes suspected of having asthma should
undergo a thorough health history examination and preparticipation physical examination. Unfortunately, the sensitivity and
specificity of the medical history are not known, and this evaluation may not be the best method for identifying asthma.14
Performing warmup activities before sport participation can
help prevent asthma attacks. With a structured warmup protocol, the athlete may experience a refractory period of as long
as 2 hours, potentially decreasing the risk of an exacerbation
or decreasing reliance on medications.6 In addition, the sports
medicine team should provide education to assist the athlete in
recognizing asthma signs and symptoms, understanding how
to use medication as prescribed (including potential adverse
effects and barriers to taking medications, which can include
failure to recognize the importance of controlling asthma,
failure to recognize the potential severity of the condition,
medication costs, difficulty obtaining medications, inability to
integrate treatment of the disease with daily life, and distrust
of the medical establishment), and using spirometry equipment
correctly.2,4,5
Recognition. Athletes with asthma may display the following signs and symptoms: confusion, sweating, drowsiness,
FEV1 of less than 40%, low level of oxygen saturation, use of
accessory muscles for breathing, wheezing, cyanosis, coughing, hypotension, bradycardia or tachycardia, mental status
Journal of Athletic Training
3
CATASTROPHIC BRAIN INJURIES
Prevention
Pr
Recommendations
In
1. The AT is responsible for coordinating educational sessions with athletes and coaches to teach the recognition
of concussion (ie, specific signs and symptoms), serious nature of traumatic brain injuries in sport, and importance of reporting concussions and not participating
while symptomatic. Evidence Category: C
2. The AT should enforce the standard use of certified helmets while also educating athletes, coaches, and parents
that although such helmets meet a standard for helping
to prevent catastrophic head injuries, they do not prevent
cerebral concussions. Evidence Category: B
Recognition
3. The AT should incorporate the use of a comprehensive
objective concussion assessment battery that includes
symptom, cognitive, and balance measures. Each of these
represents only one piece of the concussion puzzle and
should not be used in isolation to manage concussion.
Evidence Category: A
4
Treatment and Management
4. A comprehensive medical management plan for acute
care of an athlete with a potential intracranial hemorrhage or diffuse cerebral edema should be implemented.
Evidence Category: B
5. If the athlete’s symptoms persist or worsen or the level of
consciousness deteriorates after a concussion, the patient
should be immediately referred to a physician trained in
concussion management. Evidence Category: B
6. Oral and written instructions for home care should be
given to the athlete and to a responsible adult. Evidence
Category: C
7. Returning an athlete to participation after a head injury
should follow a graduated progression that begins once the
athlete is completely asymptomatic. Evidence Category: C
8. The athlete should be monitored periodically throughout
and after these sessions to determine whether any symptoms
develop or increase in intensity. Evidence Category: C
Background and Literature Review
s
Definition, Epidemiology, and Pathophysiology. Cerebral
concussion is classified as mild traumatic brain injury and often
affects athletes in both helmeted and nonhelmeted sports.18,19
The Centers for Disease Control and Prevention estimated that
1.6 to 3.8 million sport-related concussive injuries occur annually in the United States.20 Although they are rare, severe catastrophic traumatic brain injuries, such as subdural and epidural
hematomas and malignant cerebral edema (ie, second-impact
syndrome), result in more fatalities from direct trauma than any
other sport injury. When these injuries do occur, brain swelling
or pooling of blood (or both) increases intracranial pressure; if
this condition is not treated quickly, brainstem herniation and
respiratory arrest can follow. Catastrophic brain injuries rank
second only to cardiac-related injuries and illnesses as the most
common cause of fatalities in football players.21 However, the
National Center for Catastrophic Sport Injury Research reported
that fatal brain injuries have occurred in almost every sport,
including baseball, lacrosse, soccer, track, and wrestling.22 For
a catastrophic brain injury such as second-impact syndrome,
which has a mortality rate approaching 50% and a morbidity
rate nearing 100%, prevention is of the utmost importance.
Prevention. Preventing catastrophic brain injuries in sports,
such as skull fractures, intracranial hemorrhages, and diffuse
cerebral edema (second-impact syndrome), must involve the
following: (1) prevention and education about traumatic brain
injury for athletes, coaches, and parents; (2) enforcing the standard use of sport-specific and certified equipment (eg, National
Operating Committee on Standards for Athletic Equipment
[NOCSAE] or Hockey Equipment Certification Council, Inc
[HECC]–certified helmets); (3) use of comprehensive, objective baseline and postinjury assessment measures; (4) administration of home care and referral instructions emphasizing the
monitoring and management of deteriorating signs and symptoms; (5) use of systematic and monitored graduated RTP progressions; (6) clearly documented records of the evaluation and
management of the injury to help guide a sound RTP decision;
and (7) proper preparedness for on-field medical management
of a serious head injury.
Prevention begins with education. The AT is responsible for
coordinating educational sessions with athletes and coaches
to teach the recognition of concussion (ie, specific signs and
es
changes, loss of consciousness, inability to lie supine, inability to speak coherently, or agitation.2,4,5 Peak expiratory flow
rates of less than 80% of the personal best or daily variability
greater than 20% of the morning value indicate lack of control
of asthma. The sports medicine staff should consider testing all
athletes with asthma using a sport-specific and environmentspecific exercise challenge protocol to assist in determining
triggers of airway hyperresponsiveness.6
Treatment. Treatment for those with asthma includes recognition of exacerbating factors and the proper use of asthma
medications (Figure 1). A short-acting β2-agonist should be
readily available; onset of action is typically 5 to 15 minutes,
so the medication can be readministered 1 to 3 times per hour if
needed.10 If breathing difficulties continue after 3 treatments in
1 hour or the athlete continues to have any signs or symptoms
of acute respiratory distress, referral to an acute or urgent care
facility should ensue. For breathing distress, the sports medicine team should provide supplemental oxygen to help maintain blood oxygen saturation above 92%.10
Proper use of inhaled corticosteroids can decrease the frequency and severity of asthma exacerbations while improving
lung function and reducing hyperresponsiveness and the need
for short-acting β2-agonists.15,16 Leukotriene modifiers can be
used to control allergen-, aspirin-, or exercise-induced bronchoconstriction and decrease asthma exacerbations.17
Return to Play. No specific guidelines describe RTP after
an asthma attack in an athlete. However, in general, the athlete
should first be asymptomatic and progress through graded increases in exercise activity. Lung function should be monitored
with a peak flow meter and compared with baseline measures
to determine when asthma is sufficiently controlled to allow
the athlete to resume participation.11 Where possible, the sports
medicine staff should identify and treat asthmatic triggers, such
as allergic rhinitis, before the athlete returns to participation.
Volume 47 • Number 1 • February 2012
s
symptoms by those with whom the athlete lives is both important and practical. If symptoms persist or worsen or the level
of consciousness deteriorates after a concussion, the athlete
should be immediately referred to a medical facility. To assist
with this, oral and written instructions for home care should
be given to the athlete and to a responsible adult (eg, parents
or roommate) who will observe and supervise the athlete during the acute phase of the concussion while at home or in the
dormitory. The AT and physician should agree on a standard
concussion home instruction form similar to the one presented
in the NATA position statement23 and Zurich guidelines.30,31
The proper preparedness for on-field and sideline medical
management of a head injury becomes paramount if the athlete
has a more serious and quickly deteriorating condition. If the
athlete presents with a Glasgow coma score of less than 8 or
other indications of more involved brain or brainstem impairment appear (eg, posturing, altered breathing pattern), the AT or
other members of the sports medicine team must be prepared
to perform manual ventilations through either endotracheal intubation or bag-valve-mouth resuscitation. These procedures
should be initiated if the athlete is not oxygenating well (ie,
becoming dusky or blue, ventilating incompletely and slower
than normal at 12 to 15 breaths per minute).32 Additionally, the
sports medicine team should aim to reduce intracranial pressure
by elevating the head to at least 30° and ensuring that the head
and neck are maintained in the midline position to optimize
venous outflow from the brain. Hyperventilation and intravenous (IV) diuretics such as mannitol (0.5 to 1.0 g/kg) may also
decrease intracranial pressure.32 Obviously, being prepared for
immediate transfer to a medical facility is extremely important
under these conditions.
Return to Play. Once the athlete is asymptomatic, has been
cleared by a physician with training in concussion management,
and has returned to baseline on follow-up assessments, a graduated RTP protocol should begin (Table 1). If the exertional activities do not produce acute symptoms, he or she may progress
to the next step. No more than 2 steps should be performed on
the same day, which allows monitoring of both acute (during
the activity) and delayed (within 24 hours after the activity)
symptoms. The athlete may advance to step 5 and return to full
participation once he or she has remained asymptomatic for 24
hours after step 4 of the protocol. The athlete should be monitored periodically throughout and after these sessions with objective assessment measures to determine whether an increase
in intensity is warranted. If the athlete’s symptoms return at
any point during the RTP progression, at least 24 hours without
symptoms must pass before the protocol is reintroduced, beginning at step 1.
In
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es
symptoms), serious nature of traumatic brain injuries in sport,
and importance of reporting their injuries and not participating while symptomatic. During this process, athletes who are at
risk for subsequent concussion or catastrophic injury should be
identified and counseled about the risk of subsequent injury.
As recommended in the NATA position statement on management of sport-related concussion,23 the AT should enforce
the standard use of helmets for preventing catastrophic head
injuries and reducing the severity of cerebral concussions in
sports that require helmet protection (eg, football, men’s lacrosse, ice hockey, baseball, softball). The AT should ensure
that all equipment meets NOCSAE, HECC, or American Society for Testing and Materials (ASTM) standards. A poorly fitted
helmet is limited in the amount of protection it can provide, and
the AT must play a role in enforcing the proper fit and use of
the helmet. Protective sport helmets are designed primarily to
help prevent catastrophic injuries (eg, skull fractures and intracranial hematomas) and not concussions. A helmet that protects
the head from a skull fracture does not adequately prevent the
rotational and shearing forces that lead to many concussions,24
a fact that many people misunderstand.
Recognition. The use of objective concussion measures
during preseason and postinjury assessments helps the AT and
physician accurately identify deficits associated with the injury
and track recovery. However, neuropsychological testing is
only one component of the evaluation process and should not
be used as a standalone tool to diagnose or manage concussion
or to make RTP decisions after concussion. Including objective measures of cognitive function and balance prevents premature clearance of an athlete who reports being symptom free
but has persistent deficits that are not easily detected through
the clinical examination. The concussion assessment battery
should include a combination of tests for cognition, balance,
and self-reported symptoms known to be affected by concussion. Because many athletes (an estimated 49% to 75%)25,26 do
not report their concussions, this objective assessment model
is important. The sensitivity of this comprehensive battery,
including a graded symptom checklist, computerized neuropsychological test, and balance test, reached 94%,27 which is
consistent with previous reports.28,29
Multiple concussion assessment tools are available, including low-technology and high-technology balance tests, brief
paper-and-pencil cognitive tests, and computerized cognitive tests. As of 2010, the National Football League, National
Hockey League, and National Collegiate Athletic Association
require an objective assessment as part of a written concussion
management protocol. By using objective measures, which
were endorsed by the Third International Consensus Statement
on Concussion in Sport (Zurich, 2008),30,31 ATs and physicians
are better equipped to manage concussion than by relying
solely on subjective reports from the athlete. Additionally, the
often hidden deficits associated with concussion and gradual
deterioration that may indicate more serious brain trauma or
postconcussion syndrome (ie, symptoms lasting longer than 4
weeks) may be detected with these tools.
Treatment. Once the athlete has been thoroughly evaluated
and identified as having sustained a concussion, a comprehensive medical management plan should be implemented. This
begins with making a determination about whether the patient
should be immediately referred to a physician or sent home with
specific observation instructions. Although this plan should include serial evaluations and observations by the AT (as outlined
earlier), continued monitoring of postconcussion signs and
Table 1. Graduated Return-to-Play Sample Protocol
Exertion Step
1. 2. 3. 4. 5.
Activities
20-min stationary bike at 10–14 mph (16–23 kph)
Interval bike: 30-s sprint at 18–20 mph (29–32 kph),
30-s recovery × 10 repetitions; body weight circuit:
squats, push-ups, sit-ups × 20 s × 3 repetitions
60-yd (55-m) shuttle run × 10 repetitions with 40-s
rest, plyometric workout: 10-yd (9-m) bounding, 10
medicine ball throws, 10 vertical jumps × 3 repetitions;
noncontact, sport-specific drills × 15 min
Limited, controlled return to practice with monitoring
for symptoms
Full sport participation in practice
Journal of Athletic Training
5
The AT should document all pertinent information surrounding the evaluation and management of all suspected concussions, including (a) mechanism of injury; (b) initial signs and
symptoms; (c) state of consciousness; (d) findings on serial
testing of symptoms, neuropsychological function, and balance
(noting any deficits compared with baseline); (e) instructions
given to the athlete, parent, or roommate; (f) recommendations provided by the physician; (g) graduated RTP progression, including dates and specific activities involved in the
athlete’s return to participation; and (h) relevant information on
the player’s history of prior concussion and associated recovery patterns.23 This level of detail can help prevent a premature
return to participation and a catastrophic brain injury such as
second-impact syndrome.
CERVICAL SPINE INJURIES
Recommendations
Equipment-Laden Athletes
13.The primary acute treatment goals in equipment-laden
athletes are to ensure that the cervical spine is immobilized in neutral and vital life functions are accessible.
Removal of helmet and shoulder pads in any equipmentintensive sport should be deferred53–56 until the athlete
has been transported to an emergency medical facility
except in 3 circumstances57: the helmet is not properly
fitted to prevent movement of the head independent of
the helmet, the equipment prevents neutral alignment of
the cervical spine, or the equipment prevents airway or
chest access.53,54,58 Evidence Category: C
14.Full face-mask removal using established tools and techniques59–61 is executed once the decision has been made
to immobilize and transport. Evidence Category: C
15.If possible, a team physician or AT should accompany
the athlete to the hospital. Evidence Category: C
16.Remaining protective equipment should be removed by
appropriately trained professionals in the emergency department. Evidence Category: C
es
1. Athletic trainers should be familiar with sport-specific
causes of catastrophic cervical spine injury and understand the physiologic responses in spinal cord injury.
Evidence Category: C
2. Coaches and athletes should be educated about the
mechanisms of catastrophic spine injuries and pertinent
safety rules enacted for the prevention of cervical spine
injuries. Evidence Category: C
3. Corrosion-resistant hardware should be used in helmets,
helmets should be regularly maintained throughout a
season, and helmets should undergo regular reconditioning and recertification.33 Evidence Category: B
4. Emergency department personnel should become familiar with proper athletic equipment removal, seeking
education from sports medicine professionals regarding
appropriate methods to minimize motion. Evidence Category: C
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Prevention
Recognition
In
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5. During initial assessment, the presence of any of the following, alone or in combination, requires the initiation
of the spine injury management protocol: unconsciousness or altered level of consciousness, bilateral neurologic findings or complaints, significant midline spine
pain with or without palpation, or obvious spinal column
deformity.34–39 Evidence Category: A
Treatment and Management
6. The cervical spine should be in neutral position, and
manual cervical spine stabilization should be applied
immediately.40,41 Evidence Category: B
7. Traction must not be applied to the cervical spine.42,43
Evidence Category: B
8. Immediate attempts should be made to expose the airway. Evidence Category: C
9. If rescue breathing becomes necessary, the person with
the most training and experience should establish an airway and begin rescue breathing using the safest technique.44,45 Evidence Category: B
6
10.If the spine is not in a neutral position, rescuers should
realign the cervical spine.46,47 However, the presence or
development of any of the following, alone or in combination, is a contraindication to realignment45,48: pain
caused or increased by movement, neurologic symptoms, muscle spasm, airway compromise, physical difficulty repositioning the spine, encountered resistance,
or apprehension expressed by the patient. Evidence Category: B
11.Manual stabilization of the head should be converted to
immobilization using external devices such as foam head
blocks.47,49 Whenever possible, manual stabilization50 is
resumed after the application of external devices. Evidence Category: B
12.Athletes should be immobilized with a long spine board
or other full-body immobilization device.51,52 Evidence
Category: B
Volume 47 • Number 1 • February 2012
Background and Literature Review
Definition, Epidemiology, and Pathophysiology. A catastrophic cervical spinal cord injury occurs with structural distortion of the cervical spinal column and is associated with
actual or potential damage to the spinal cord.62 The spinal injury that carries the greatest risk of immediate sudden death
for the athlete occurs when the damage is both severe enough
and at a high enough level in the spinal column (above C5) to
affect the spinal cord’s ability to transmit respiratory or circulatory control from the brain.63,64 The priority in these situations
is simply to support the basic life functions of breathing and
circulation. Unfortunately, even if an athlete survives the initial
acute management phase of the injury, the risk of death persists
because of the complex biochemical cascade of events that occurs in the injured spinal cord during the initial 24 to 72 hours
after injury.64 Because of this risk, efficient acute care, transport, diagnosis, and treatment are critical in preventing sudden
death in a patient with a catastrophic cervical spine injury.
Treatment and Management. A high level of evidence (ie,
prospective randomized trials) on this topic is rare, and technology, equipment, and techniques will continue to evolve, but
DIABETES MELLITUS
Recommendations
Prevention
Treatment and Management
7. Mild hypoglycemia (ie, the athlete is conscious and able
to swallow and follow directions) is treated by administering approximately 10–15 g of carbohydrates (examples include 4–8 glucose tablets or 2 tablespoons of
honey) and reassessing blood glucose levels immediately and 15 minutes later. Evidence Category: C
8. Severe hypoglycemia (ie, the athlete is unconscious or
unable to swallow or follow directions) is a medical
emergency, requiring activation of emergency medical
services (EMS) and, if the health care provider is properly trained, administering glucagon. Evidence Category: C
9. Athletic trainers should follow the ADA guidelines for
athletes exercising during hyperglycemic periods. Evidence Category: C
10.Physicians should determine a safe blood glucose range
to return an athlete to play after an episode of mild hypoglycemia or hyperglycemia. Evidence Category: C
Background and Literature Review
Definition, Epidemiology, and Pathophysiology. Diabetes
mellitus is a chronic metabolic disorder characterized by hyperglycemia, caused by either absolute insulin deficiency or
resistance to the action of insulin at the cellular level, which
results in the inability to regulate blood glucose levels within
the normal range of 70–110 mg/dL. Type 1 diabetes is an autoimmune disorder stemming from a combination of genetic and
environmental factors. The autoimmune response is often triggered by an environmental event, such as a virus, and it targets
the insulin-secreting beta cells of the pancreas. When beta cell
mass is reduced by approximately 80%, the pancreas is no longer able to secrete sufficient insulin to compensate for hepatic
glucose output.67,68
Prevention. Although the literature supports physical activity for people with type 1 diabetes, exercise training and
competition can result in major disturbances to blood glucose
management. Extreme glycemic fluctuations (severe hypoglycemia or hyperglycemia with ketoacidosis) can lead to sudden
death in athletes with type 1 diabetes mellitus.69–71 Prevention of these potentially life-threatening events begins with
the creation of the diabetes care plan by a physician. The plan
should identify blood glucose targets for practices and games,
including exclusion thresholds; strategies to prevent exerciseassociated hypoglycemia, hyperglycemia, and ketosis; a list of
medications used for glycemic control; signs, symptoms, and
treatment protocols for hypoglycemia, hyperglycemia, and ketosis; and emergency contact information.72
Preventing hypoglycemia relies on a 3-pronged approach of
frequent blood glucose monitoring, carbohydrate supplementation, and insulin adjustments. The athlete should check blood
glucose levels 2 or 3 times before, every 30 minutes during,
and every other hour up to 4 hours after exercise. Carbohydrates should be eaten before, during, and after exercise; the
quantity the athlete ingests depends on the prevailing blood
Recognition
In
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es
1. Each athlete with diabetes should have a diabetes care
plan that includes blood glucose monitoring and insulin
guidelines, treatment guidelines for hypoglycemia and
hyperglycemia, and emergency contact information. Evidence Category: C
2. Prevention strategies for hypoglycemia include blood
glucose monitoring, carbohydrate supplementation, and
insulin adjustments. Evidence Category: B
3. Prevention strategies for hyperglycemia are described by
the American Diabetes Association (ADA) and include
blood glucose monitoring, insulin adjustments, and urine
testing for ketone bodies.67 Evidence Category: C
the breath, unusual fatigue, sleepiness, loss of appetite,
increased thirst, and frequent urination. Evidence Category: C
s
the primary goals offered in the NATA position statement on
acute management of the cervical spine–injured athlete65 remain the same: create as little motion as possible and complete
the steps of the EAP as rapidly as is appropriate to facilitate
support of basic life functions and prepare for transport to the
nearest emergency treatment facility.
Additional complications can affect the care of the spineinjured athlete in an equipment-intensive sport when rescuers
may need to remove protective equipment that limits access to
the airway or chest. Knowing how to deal properly with protective equipment during the immediate care of an athlete with
a potential catastrophic cervical spine injury can greatly influence the outcome. Regardless of the sport or the equipment,
2 principles should guide management of the equipment-laden
athlete with a potential cervical spine injury:
1. Exposure and access to vital life functions (eg, airway,
chest for CPR, or use of an AED) must be established or
easily achieved in a reasonable and acceptable manner.
2. Neutral alignment of the cervical spine should be maintained while allowing as little motion at the head and
neck as possible.
Return to Play. Return to play after cervical spine injury is
highly variable and may be permitted only after complete tissue healing, neurologic recovery, and clearance by a physician.
Factors considered for RTP include the level of injury, type of
injury, number of levels fused for stability, cervical stenosis,
and activity.66
4. Hypoglycemia typically presents with tachycardia,
sweating, palpitations, hunger, nervousness, headache,
trembling, or dizziness; in severe cases, loss of consciousness and death can occur. Evidence Category: C
5. Hyperglycemia can present with or without ketosis.
Typical signs and symptoms of hyperglycemia without
ketosis include nausea, dehydration, reduced cognitive
performance, feelings of sluggishness, and fatigue. Evidence Category: C
6. Hyperglycemia with ketoacidosis may include the signs
and symptoms listed earlier as well as Kussmaul breathing (abnormally deep, very rapid sighing respirations
characteristic of diabetic ketoacidosis), fruity odor to
Journal of Athletic Training
7
Table 2. Treatment Guidelines for Mild and Severe Hypoglycemia76,77
Mild Hypoglycemia
Severe Hypoglycemia
1. Give 10–15 g of fast-acting carbohydrate. Example: 4–8 glucose
tablets, 2 Tbsp honey.
2. Measure blood glucose level.
3. Wait 15 min and remeasure blood glucose level.
4. If blood glucose level remains low, administer another 10–15 g of
fast-acting carbohydrate.
5. Recheck blood glucose level in 15 min.
6. If blood glucose level does not return to normal after second dose
of carbohydrate, activate EMS.
7. Once blood glucose level normalizes, provide a snack (eg,
sandwich, bagel).
1. Activate EMS.
2. Prepare glucagon for injection, following directions in glucagon kit.
3. Once athlete is conscious and able to swallow, provide food.
Abbreviation: EMS, emergency medical services. Revised with permission from Jimenez CC, Corcoran MH, Crawley JT, et al. National Athletic
Trainers’ Association position statement: management of the athlete with type I diabetes mellitus. J Athl Train. 2007;42(4):536–545.
s
2.82,83 The ADA provides guidelines for exercise during hyperglycemic periods. If the fasting blood glucose level is ≥250 mg/
dL (≥13.9 mmol/L), the athlete should test his or her urine for
the presence of ketones. If ketones are present, exercise is contraindicated. If the blood glucose value is ≥300 mg/dL (≥16.7
mmol/L) and without ketones, the athlete may exercise with
caution and continue to monitor blood glucose levels. Athletes
should work with their physicians to determine the need for insulin adjustments for periods of hyperglycemia before, during,
and after exercise.67
Return to Play. The literature does not address specific RTP
guidelines after hypoglycemic or hyperglycemic events. Therefore, RTP for an athlete varies with the individual and becomes
easier as the AT works with the athlete on a regular basis and
learns how his or her blood glucose reacts to exercise and insulin and glucose doses. The athlete should demonstrate a stable
blood glucose level that is within the normal range before RTP.
Athletic trainers working with new athletes should seek guidance from the athlete, athlete’s physician, and athlete’s parents
to gain insight on how the athlete has been able to best control
the blood glucose level during exercise.
In
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glucose level and exercise intensity. Finally, some athletes may
use insulin adjustments to prevent hypoglycemia. These adjustments vary depending on the method of insulin delivery (insulin pump versus multiple daily injections), prevailing blood
glucose level, and exercise intensity.67,68,73,74
Athletes with type 1 diabetes may also experience hyperglycemia, with or without ketosis, during exercise. Hyperglycemia
during exercise is related to several factors, including exercise
intensity75,76 and the psychological stress of competition.77 When
the insulin level is adequate, these episodes of hyperglycemia
are transient. However, when the insulin level is insufficient,
ketosis can occur. Exercise is contraindicated when ketones
are present in the urine. Athletic trainers should know the ADA
guidelines for athletes exercising during an episode of hyperglycemia.67 In addition, the athlete’s physician should determine
the need for insulin adjustments during hyperglycemic periods.
Recognition. Signs and symptoms of hypoglycemia typically occur when blood glucose levels fall below 70 mg/dL
(3.9 mmol/L). Early symptoms include tachycardia, sweating,
palpitations, hunger, nervousness, headache, trembling, and
dizziness. These symptoms are related to the release of epinephrine and acetylcholine. As the glucose level continues to
fall, symptoms of brain neuronal glucose deprivation occur, including blurred vision, fatigue, difficulty thinking, loss of motor control, aggressive behavior, seizures, convulsions, and loss
of consciousness. If hypoglycemia is prolonged, severe brain
damage and even death can occur. Athletic trainers should be
aware that the signs and symptoms of hypoglycemia are individualized and be prepared to act accordingly.78–80
Although the signs and symptoms of hypoglycemia may
vary from one athlete to another, they include nausea, dehydration, reduced cognitive performance, slowing of visual reaction
time, and feelings of sluggishness and fatigue. The signs and
symptoms of hyperglycemia with ketoacidosis may include
those listed earlier as well as Kussmaul breathing, fruity odor
to the breath, sleepiness, inattentiveness, loss of appetite, increased thirst, and frequent urination. With severe ketoacidosis,
the level of consciousness may be reduced. Athletic trainers
should also be aware that some athletes with type 1 diabetes
intentionally train and compete in a hyperglycemic state (above
180 mg/dL [10 mmol/L]) to avoid hypoglycemia. Competing in
a hyperglycemic state places the athlete at risk for dehydration,
reduced athletic performance, and possibly ketosis.67,81
Treatment and Management. Treatment guidelines for
mild and severe cases of hypoglycemia are shown in Table
8
Volume 47 • Number 1 • February 2012
EXERTIONAL HEAT STROKE
Recommendations
Prevention
1. In conjunction with preseason screening, athletes should
be questioned about risk factors for heat illness or a history of heat illness. Evidence Category: C
2. Special considerations and modifications are needed for
those wearing protective equipment during periods of
high environmental stress. Evidence Category: B
3. Athletes should be acclimatized to the heat gradually
over a period of 7 to 14 days. Evidence Category: B
4. Athletes should maintain a consistent level of euhydration and replace fluids lost through sweat during games
and practices. Athletes should have free access to readily
available fluids at all times, not only during designated
breaks. Evidence Category: B
5. The sports medicine staff must educate relevant personnel (eg, coaches, administrators, security guards, EMS
staff, athletes) about preventing exertional heat stroke
(EHS) and the policies and procedures that are to be followed in the event of an incident. Signs and symptoms of
Recognition
6. The 2 main criteria for diagnosis of EHS are (1) core
body temperature of greater than 104° to 105°F (40.0°
to 40.5°C) taken via a rectal thermometer soon after collapse and (2) CNS dysfunction (including disorientation,
confusion, dizziness, vomiting, diarrhea, loss of balance,
staggering, irritability, irrational or unusual behavior, apathy, aggressiveness, hysteria, delirium, collapse, loss of
consciousness, and coma). Evidence Category: B
7. Rectal temperature and gastrointestinal temperature (if
available) are the only methods proven valid for accurate
temperature measurement in a patient with EHS. Inferior
temperature assessment devices should not be relied on
in the absence of a valid device. Evidence Category: B
Treatment
Background and Literature Review
es
8. Core body temperature must be reduced to less than
102°F (38.9°C) as soon as possible to limit morbidity and
mortality. Cold-water immersion is the fastest cooling
modality. If that is not available, cold-water dousing or wet
ice towel rotation may be used to assist with cooling, but
these methods have not been shown to be as effective as
cold- water immersion. Athletes should be cooled first and
then transported to a hospital unless cooling and proper
medical care are unavailable onsite. Evidence Category: B
9. Current suggestions include a period of no activity, an
asymptomatic state, and normal blood enzyme levels before the athlete begins a gradual return-to-activity progression under direct medical supervision. This progression should start at low intensity in a cool environment
and slowly advance to high-intensity exercise in a warm
environment. Evidence Category: C
In
Pr
Definition, Epidemiology, and Pathophysiology. Exertional heat stroke is classified as a core body temperature of
greater than 104° to 105°F (40.0° to 40.5°C) with associated
CNS dysfunction.84–87 The CNS dysfunction may present as
disorientation, confusion, dizziness, vomiting, diarrhea, loss
of balance, staggering, irritability, irrational or unusual behavior, apathy, aggressiveness, hysteria, delirium, collapse, loss of
consciousness, and coma. Other signs and symptoms that may
be present are dehydration, hot and wet skin, hypotension, and
hyperventilation. Most athletes with EHS will have hot, sweaty
skin as opposed to the dry skin that is a manifestation of classical EHS.84,85,88,89
Although it is usually among the top 3 causes of death in
athletes, EHS may rise to the primary cause during the summer.89 The causes of EHS are multifactorial, but the ultimate result is an overwhelming of the thermoregulatory system, which
causes a buildup of heat within the body.84,90–92
Prevention. Exercise intensity can increase core body temperature faster and higher than any other factor.85 Poor physical
condition is also related to intensity. Athletes who are less fit
than their teammates must work at a higher intensity to produce
the same outcome. Therefore, it is important to alter exercise
intensity and rest breaks when environmental conditions are
dangerous.93
As air temperature increases, thermal strain increases, but
if relative humidity increases as well, the body loses its ability
to use evaporation as a cooling method (the main method used
during exercise in the heat).87,94–97 Adding heavy or extensive
protective equipment also increases the potential risk, not only
because of the extra weight but also as a barrier to evaporation
and cooling. Therefore, extreme or new environmental conditions should be approached with caution and practices altered
and events canceled as appropriate.
Acclimatization is a physiologic response to repeated heat
exposure during exercise over the course of 10 to 14 days.90,98
This response enables the body to cope better with thermal
stressors and includes increases in stroke volume, sweat output,
sweat rate, and evaporation of sweat and decreases in heart rate,
core body temperature, skin temperature, and sweat salt losses.90
Athletes should be allowed to acclimatize to the heat before
stressful conditions such as full equipment, multiple practices
within a day, or performance trials are implemented.91,93
Hydration can help reduce heart rate, fatigue, and core body
temperature while improving performance and cognitive functioning.96–98 Dehydration of as little as 2% of body weight has
a negative effect on performance and thermoregulation.87 Caution should be taken to ensure that athletes arrive at practice
euhydrated (eg, having reestablished their weight since the
last practice) and maintain or replace fluids that are lost during
practice.
Assessment. The 2 main diagnostic criteria for EHS are
CNS dysfunction and a core body temperature of greater than
104° to 105°F (40.0° to 40.5°C).99–101 The only accurate measurements of core body temperature are via rectal thermometry
or ingestible thermistors.102 Other devices, such as oral, axillary, aural canal, and temporal artery thermometers, are inaccurate methods of assessing body temperature in an exercising
person. A delay in accurate temperature assessment must also
be considered during diagnosis and may explain body temperatures that are lower than expected. Lastly, in some cases
of EHS, the patient has a lucid interval during which he or
she is cognitively normal, followed by rapidly deteriorating
symptoms.86
Due to policy and legal concerns in some settings, obtaining rectal temperature may not be feasible. Because immediate
treatment is critical in EHS, it is important to not waste time
by substituting an invalid method of temperature assessment.
Instead, the practitioner should rely on other key diagnostic indicators (eg, CNS dysfunction, circumstances of the collapse).
If EHS is suspected, cold-water immersion should be initiated
at once. The evidence strongly indicates that in patients with
suspected EHS, prompt determination of rectal temperature
followed by aggressive, whole-body cold-water immersion
maximizes the chances for survival. Practitioners in settings
in which taking rectal temperature is a concern should consult
with their administrators in advance. Athletic trainers, in conjunction with their supervising physicians, should clearly communicate to their administrators the dangers of skipping this
important step and should obtain a definitive ruling on how to
proceed in this situation.
Treatment. The goal for any EHS victim is to lower the
body temperature to 102°F (38.9°C) or less within 30 minutes
of collapse. The length of time body temperature is above the
critical core temperature (~105°F [40.5°C]) dictates any morbidity and the risk of death from EHS.103 Cold-water immersion is the most effective cooling modality for patients with
EHS.104,105 The water should be approximately 35°F (1.7°C) to
s
a medical emergency should also be reviewed. Evidence
Category: C
Journal of Athletic Training
9
Recognition
6. Athletic trainers should recognize EH signs and symptoms during or after exercise, including overdrinking,
nausea, vomiting, dizziness, muscular twitching, peripheral tingling or swelling, headache, disorientation,
altered mental status, physical exhaustion, pulmonary
edema, seizures, and cerebral edema. Evidence Category: B
7. In severe cases, EH encephalopathy can occur and the
athlete may present with confusion, altered CNS function, seizures, and a decreased level of consciousness.
Evidence Category: B
8. The AT should include EH in differential diagnoses until
confirmed otherwise. Evidence Category: C
Treatment and Management
9. If an athlete’s mental status deteriorates or if he or she
initially presents with severe symptoms of EH, IV hypertonic saline (3% to 5%) is indicated. Evidence Category: B
10.Athletes with mild symptoms, normal total body water
volume, and a mildly altered blood sodium level (130 to
135 mEq/L; normal is 135 to 145 mEq/L) should restrict
fluids and consume salty foods or a small volume of oral
hypertonic solution (eg, 3 to 5 bouillon cubes dissolved
in 240 mL of hot water). Evidence Category: C
11.The athlete with severe EH should be transported to an
advanced medical facility during or after treatment. Evidence Category: B
12.Return to activity should be guided by a plan to avoid future EH episodes, specifically an individualized hydration plan, as described earlier. Evidence Category: C
s
59°F (15.0°C) and continuously stirred to maximize cooling.
The athlete should be removed when core body temperature
reaches 102°F (38.9°) to prevent overcooling. If appropriate
medical care is available, cooling should be completed before
the athlete is transported to a hospital. If cold-water immersion is not available, other modalities, such as wet ice towels
rotated and placed over the entire body or cold-water dousing
with or without fanning, may be used but are not as effective.
Policies and procedures for cooling athletes before transport to
the hospital must be explicitly clear and shared with potential
EMS responders, so that treatment by all medical professionals
involved with a patient with EHS is coordinated.
Return to Play. Structured guidelines for RTP after EHS
are lacking. The main considerations are treating any associated sequelae and, if possible, identifying the cause of the EHS,
so that future episodes can be prevented. Many patients with
EHS are cooled effectively and sent home the same day; they
may be able to resume modified activity within 1 to 3 weeks.
However, when treatment is delayed, patients may experience
residual complications for months or years after the event.
Most guidelines suggest that the athlete be asymptomatic with
normal blood work (renal and hepatic panels, electrolytes, and
muscle enzyme levels) before a gradual return to activity is initiated.106 Unfortunately, no evidence-based tools are available to
determine whether the body’s thermoregulatory system is fully
recovered. In summary, in all cases of EHS, after the athlete has
completed a 7-day rest period and obtained normal blood work
and physician clearance, he or she may begin a progression of
physical activity, supervised by the AT, from low intensity to
high intensity and increasing duration in a temperate environment, followed by the same progression in a warm to hot environment. The ability to progress depends largely on the treatment
provided, and in some rare cases full recovery may not be possible. If the athlete experiences any side effects or negative
symptoms with training, the progression should be slowed or
delayed.
es
Background and Literature Review
EXERTIONAL HYPONATREMIA
Prevention
Pr
Recommendations
In
1. Each physically active person should establish an individualized hydration protocol based on personal sweat
rate, sport dynamics (eg, rest breaks, fluid access),
environmental factors, acclimatization state, exercise
duration, exercise intensity, and individual preferences.
Evidence Category: B
2. Athletes should consume adequate dietary sodium at
meals when physical activity occurs in hot environments. Evidence Category: B
3. Postexercise rehydration should aim to correct fluid loss
accumulated during activity. Evidence Category: B
4. Body weight changes, urine color, and thirst offer cues
to the need for rehydration. Evidence Category: A
5. Most cases of exertional hyponatremia (EH) occur in endurance athletes who ingest an excessive amount of hypotonic fluid. Athletes should be educated about proper
fluid and sodium replacement during exercise. Evidence
Category: C
10
Volume 47 • Number 1 • February 2012
Definition, Epidemiology, and Pathophysiology. Exertional hyponatremia is a rare condition defined as a serum
sodium concentration less than 130 mEq/L.107 Although no incidence data are available from organized athletics, the condition
is seen in fewer than 1% of military athletes108 and up to 30% of
distance athletes.107,109 Signs and symptoms of EH include overdrinking, nausea, vomiting, dizziness, muscular twitching, peripheral tingling or swelling, headache, disorientation, altered
mental status, physical exhaustion, pulmonary edema, seizures,
and cerebral edema. If not treated properly and promptly, EH is
potentially fatal because of the encephalopathy. Low serum sodium levels are identified more often in females than in males
and during activity that exceeds 4 hours in duration.107,110 Two
common, often additive scenarios occur when an athlete ingests hypotonic beverages well beyond sweat losses (ie, water
intoxication) or an athlete’s sweat sodium losses are not adequately replaced.111–114 Water intoxication causes low serum sodium levels because of a combination of excessive fluid intake
and inappropriate body water retention. Insufficient sodium
replacement causes low serum sodium levels when high sweat
sodium content leads to decreased serum sodium levels (which
may occur over 3 to 5 days). In both scenarios, EH causes intracellular swelling due to hypotonic intravascular and extracellular fluids. This, in turn, leads to potentially fatal neurologic and
s
EH onsite is the use of a handheld analyzer, which can identify
the serum sodium concentration within minutes.113,114 Athletic
trainers should work with physicians and EMS to maximize access to these analyzers when EH is likely.
A collapsed, semiconscious, or unconscious athlete should be
evaluated for all potential causes of sudden death in sport. The
key to the differential diagnosis of EH is serum sodium assessment, which should be conducted when EH is suspected.113,114
If a portable serum sodium analyzer is not available, it is then
necessary to rule out other conditions that may warrant onsite
treatment (eg, EHS) before emergency transport.91
Treatment. If the athlete’s mental status deteriorates or if he
or she initially presents with severe symptoms, IV hypertonic
saline (3% to 5%) is indicated.91,113,114 Intravenous hypertonic
saline rapidly corrects the symptoms of EH and decreases intracellular fluid volume. Serial measures of blood sodium should
be obtained throughout treatment (after every 100 mL of IV
fluid). To avoid complications, hypertonic saline administration
should be discontinued when the serum sodium concentration
reaches 128 to 130 mEq/L.114 Normal saline (0.9% NaCl) IV
fluids should not be provided to patients without prior serum
sodium assessment.113,114 Ideally, the ATs have discussed with
EMS in the off-season the importance of having a portable sodium analyzer available and being ready to administer hypertonic saline during transport.
Athletes with mild symptoms, normal total body water volume, and a mildly altered blood sodium concentration (130 to
135 mEq/L) should restrict fluids and consume salty foods or
a small volume of oral hypertonic solution (eg, 3 to 5 bouillon
cubes dissolved in 240 mL of hot water). This can be continued
until diuresis and correction of the blood sodium concentration
occur; such management may take hours to complete, but it is
successful in stable patients.114
The patient with severe EH should be transported to an
advanced medical facility during or after treatment. Once the
patient arrives at the emergency department, a plasma osmolality assessment is performed to identify hypovolemia or hypervolemia. Patients with persistent hypovolemia despite normal
serum sodium values should receive 0.9% NaCl IV until euvolemia is reached. The progress of symptoms and blood sodium levels determines the follow-up care.119
Return to Play. When EH is treated appropriately with IV
hypertonic saline, chronic morbidity is rare. Literature documenting the expected time course of recovery after EH is lacking, but recovery seems to depend on the severity and duration
of brain swelling. Rapid recognition and prompt treatment reduce the risk of CNS damage.120
Return to activity should be guided by a plan to avoid future EH episodes, specifically an individualized hydration plan
(documented earlier).94,115 This plan should also be based on the
history and factors that contributed to the initial EH episode.
In
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physiologic dysfunction. When physically active people match
fluid and sodium losses, via sweat and urine, with overall intake, EH is prevented.94,115 Successful treatment of EH involves
rapid sodium replacement in sufficient concentrations via foods
containing high levels of sodium (minor cases) or hypertonic
saline IV infusion (for moderate or severe cases).
Prevention. Exertional hyponatremia is most effectively
prevented when individualized hydration protocols are used
for the physically active, including hydration before, during,
and after exercise.94,115 This strategy should take into account
sweat rate, sport dynamics (eg, rest breaks, fluid access), environmental factors, acclimatization state, exercise duration, exercise intensity, and individual preferences. The strategy should
guide hydration before, during, and after activity to approximate sweat losses but ensure that fluids are not consumed in excess. This goal can be achieved by calculating individual sweat
rates (sweat rate = pre-exercise body weight – postexercise body
weight + fluid intake + urine volume/exercise time, in hours) for
a representative range of environmental conditions and exercise
intensities. Suggestions for expediting this procedure can be
found in the NATA position statement on fluid replacement.94
Sweat rate calculation is the most fundamental consideration
when establishing a rehydration protocol. Average sweat rates
from the scientific literature or other athletes vary from 0.5 L/h
to more than 2.5 L/h.115
Dietary sodium is important for normal body maintenance
of fluid balance and can help prevent muscle cramping, heat
exhaustion, and EH.91 The AT should encourage adequate dietary sodium intake, especially when athletes are training in a
hot environment and as a part of daily meals.116 Sport drinks
generally contain low levels of sodium relative to blood and
do little to attenuate decreases in whole-body sodium levels.
Instead, athletes should consume foods that are high in sodium
(eg, canned soups, pretzels) during meals before and after exercise. Including sodium in fluid-replacement beverages should
be considered under the following conditions: inadequate access to meals, physical activity exceeding 2 hours in duration,
and during the initial days to weeks of hot weather.94,115 Under
these conditions, adding salt in amounts of 0.3 to 0.7 g/L can
offset salt losses in sweat and minimize medical events associated with electrolyte imbalances.
Postexercise hydration should aim to correct the fluid loss
accumulated during activity.94,115 Ideally completed within 2
hours, rehydration fluids should contain water, carbohydrates
to replenish glycogen stores, and electrolytes to speed rehydration. When rehydration must be rapid (within 2 hours), the
athlete should compensate for obligatory urine losses incurred
during the rehydration process and drink about 25% more than
sweat losses to ensure optimal hydration 4 to 6 hours after the
event.117 However, athletes should not drink enough to gain
weight beyond pre-exercise measurements.94,115,116
Body weight changes, urine color, and thirst offer cues to
the need for rehydration.118 When preparing for an event, an
athlete should know his or her sweat rate and pre-exercise hydration status and develop a rehydration plan (discussed in detail in the recommendations).94,115 If the athlete’s specific needs
are unknown, the athlete should not drink beyond thirst.
Recognition. The AT should recognize and the physically
active should be educated on EH signs and symptoms during
exercise.113,114,116 After an exercise bout or competition, symptoms of EH may appear immediately or gradually progress
over several hours. The most efficient method of diagnosing
EXERTIONAL SICKLING
Recommendations
Prevention
1. The AT should educate coaches, athletes, and, as warranted, parents about complications of exertion in the athlete with sickle cell trait (SCT). Evidence Category: C
Journal of Athletic Training
11
Recognition
4. Screening for SCT, by self-report, is a standard component of the preparticipation physical evaluation (PPE)
monograph. Testing for SCT, when included in the PPE
or conducted previously, confirms SCT status. Evidence
Category: A
5. The AT should know the signs and symptoms of exertional sickling, which include muscle cramping, pain,
swelling, weakness, and tenderness; inability to catch
one’s breath; and fatigue, and be able to differentiate exertional sickling from other causes of collapse. Evidence
Category: C
6. The AT should understand the usual settings for and patterns of exertional sickling. Evidence Category: C
Treatment
Pr
es
7. Signs and symptoms of exertional sickling warrant immediate withdrawal from activity. Evidence Category: C
8. High-flow oxygen at 15 L/min with a nonrebreather face
mask should be administered. Evidence Category: C
9. The AT should monitor vital signs and activate the EAP
if vital signs decline. Evidence Category: C
10.Sickling collapse should be treated as a medical emergency. Evidence Category: C
11.The AT has a duty to make sure the athlete’s treating
physicians are aware of the presence of SCT and prepared to treat the metabolic complications of explosive
rhabdomyolysis. Evidence Category: B
training progression that allows longer periods of rest and recovery between repetitions.123,125 Strength and conditioning
programs may increase preparedness but must be sport specific.
Athletes with SCT should be excluded from participation in
performance tests, such as mile runs and serial sprints, because
several deaths have occurred in this setting.124 Cessation of
activity with the onset of symptoms is essential to avoid escalating a sickling episode (eg, muscle cramping, pain, swelling, weakness, and tenderness; inability to catch one’s breath;
fatigue).123,125 In general, when athletes with SCT set their own
pace, they seem to do well.123,125 Therefore, athletes with SCT
who perform repetitive high-speed sprints, distance runs, or interval training that induces high levels of lactic acid as a component of a sport-specific training regimen should be allowed
extended recovery between repetitions because this type of
conditioning poses special risks to them.123,125
Factors such as ambient heat stress, dehydration, asthma, illness, and altitude predispose the athlete with SCT to a crisis
during physical exertion, even when exercise is not all-out.123,125
Extra precautions are warranted in these conditions. These precautions may include the following:
• Work-rest cycles should be adjusted for environmental
heat stress.
• Hydration should be emphasized.
• Asthma should be controlled.
• The athlete with SCT who is ill should not work out.
• The athlete with SCT who is new to a high-altitude environment should be watched closely. Training should be
modified and supplemental oxygen should be available
for competitions.
One last precaution is to create an environment that encourages athletes with SCT to immediately report any signs or
symptoms such as leg or low back cramping, difficulty breathing, or fatigue. Such signs and symptoms in an athlete with
SCT should be assumed to represent sickling.123
Recognition. The PPE monograph14 recommends screening for SCT with the question, “Do you or [does] someone in
your family have SCT or disease?” Small numbers of affected
athletes limit the collection of sufficient evidence to support
testing for SCT in the PPE. However, because PPE medical
history form answers are highly suspect126 and deaths can be
tied to a lack of awareness about SCT, the argument for testing
to confirm trait status remains strong. The National Collegiate
Athletic Association currently mandates testing for SCT. Irrespective of testing, the AT should educate staff, coaches, and
athletes on the potentially lethal nature of this condition.123 Education and precautions work best when targeted at the athletes
most at risk. Incidence rates of SCT are approximately 8% in
African Americans, 0.5% in Hispanics, and 0.2% in whites (but
more common in those from the Mediterranean, the Middle
East, and India).127
Not all athletes who experience sickling present the same
way. The primary limiting symptoms are leg or low back cramps
or spasms, weakness, debilitating low back pain,128 difficulty
recovering (“I can’t catch my breath”), and fatigue. Sickling
often lacks a prodrome, so these symptoms in an athlete with
SCT should be treated as exertional sickling.123
Sickling collapse has been mistaken for cardiac collapse or
heat illness.129 However, unlike sickling collapse, cardiac collapse tends to be instantaneous, is not associated with cramping, and results in the athlete hitting the ground without any
protective reflex mechanism and being unable to talk. Also unlike sickling collapse, heat illness collapse often occurs after a
s
2. Targeted education and tailored precautions may provide
a margin of safety for the athlete with SCT. Evidence
Category: C
3. Athletes with known SCT should be allowed longer
periods of rest and recovery between conditioning repetitions, be excluded from participation in performance
tests such as mile runs and serial sprints, adjust workrest cycles in the presence of environmental heat stress,
emphasize hydration, control asthma (if present), not
work out if feeling ill, and have supplemental oxygen
available for training or competition when new to a
high-altitude environment. Evidence Category: B
Background and Literature Review
In
Prevention. No contraindications to participation in sport
exist for the athlete with SCT.121–123 Recognition of the athlete’s
positive SCT status must be followed with targeted education and tailored precautions because deaths have been tied to
lapses in education and inadequate precautions.124 The athlete
with SCT should be informed that SCT is consistent with a
normal, healthy life span, although associated complications
may occur. Education should include genetic considerations
with respect to family planning and questioning about any past
medical history of sickling events. Athletes and staff should be
educated about the signs, symptoms, and settings of exertional
sickling and precautions for the athlete with SCT.123
The premise behind the suggested precautions is that exertional sickling can be brought about through intense, sustained
activity with modifiers that increase the intensity.125 One precaution that can mitigate exertional sickling is a slow, paced
12
Volume 47 • Number 1 • February 2012
5. The AT should inform treating physicians of the athlete’s trait status so that they are prepared to treat explosive rhabdomyolysis and associated metabolic
complications.124,125,129,131,132
6. Proactively prepare by having an EAP and appropriate
emergency equipment available.
Return to Play. After nonfatal sickling, the athlete may return to sport the same day or be disqualified from further participation. Athletes whose conditions are identified quickly and
managed appropriately may return the same day as symptoms
subside. Others have self-limiting myalgia from myonecrosis in
moderate rhabdomyolysis and may need 1 to 2 weeks of recovery with serial assessments.122 Patients with severe rhabdomyolysis necessitating dialysis and months of hospitalization133
may not RTP due to diminished renal function, muscle lost to
myonecrosis, or neuropathy from compartment syndrome.121
As with any RTP after a potential deadly incident, it is imperative that the physician, AT, coach, and athlete work in concert
to ensure the athlete’s safety and minimize risk factors that may
have caused the initial incident.
HEAD-DOWN CONTACT IN FOOTBALL
Recommendations
Prevention
s
1. Axial loading is the primary mechanism for catastrophic
cervical spine injury. Head-down contact, defined as initiating contact with the top or crown of the helmet, is
the only technique that results in axial loading. Evidence
Category: A
2. Spearing is the intentional use of a head-down contact
technique. Unintentional head-down contact is the inadvertent dropping of the head just before contact. Both
head-down techniques are dangerous and may result in
axial loading of the cervical spine and catastrophic injury. Evidence Category: A
3. Football helmets and other standard football equipment
do not cause or prevent axial-loading injuries of the cervical spine. Evidence Category: A
4. Injuries that occur as a result of head-down contact are
technique related and are preventable to the extent that
head-down contact is preventable. Evidence Category:
C
5. Making contact with the shoulder or chest while keeping
the head up greatly reduces the risk of serious head and
neck injury. With the head up, the player can see when
and how impact is about to occur and can prepare the
neck musculature. Even if head-first contact is inadvertent, the force is absorbed by the neck musculature, the
intervertebral discs, and the cervical facet joints. This is
the safest contact technique. Evidence Category: C
6. The game can be played as aggressively with the head
up and with shoulder contact but with much less risk of
serious injury (Figure 2). However, the technique must
be learned, and to be learned, it must be practiced extensively. Athletes who continue to drop their heads just before contact need additional coaching and practice time.
Evidence Category: C
7. Initiating contact with the face mask is a rule violation
and must not be taught. If the athlete uses poor technique
by lowering his head, he places himself in the head-
In
Pr
es
moderate but still intense bout of exercise, usually more than
30 minutes in duration. In addition, the athlete will have a core
body temperature >104°F (40.0°C). Alternatively, sickling collapse typically occurs within the first half hour on the field, and
core temperature is not greatly elevated.129,130
Sickling is often confused with heat cramping but may be
differentiated by the following:
• Heat cramping often has a prodrome of muscle twinges;
sickling has none.
• Heat-cramping pain is more excruciating and can be pinpointed, whereas sickling cramping is more generalized
but still strong.
• Those with heat cramps hobble to a halt with “locked-up”
muscles, whereas sickling athletes slump to the ground
with weak muscles. Many times, sickling athletes push
through several instances of collapse before being unable
to continue.
• Those with heat cramps writhe and yell in pain; their
muscles are visibly contracted and rock hard. Those who
are sickling lie fairly still, not yelling in pain, with muscles that look and feel normal to the observer.
Certain factors are common in severe or fatal exertional
sickling collapses. These cases tend to be similar in setting and
syndrome and are characterized by the following:
• Sickling athletes may be on the field only briefly before
collapsing, sprinting only 800 to 1600 meters, often early
in the season.
• Sickling can occur during repetitive running of hills or
stadium steps, during intense, sustained strength training;
if the tempo increases toward the end of intense 1-hour
drills; and at the end of practice when athletes run “gassers.” Sickling occurs rarely in competition, most often
in athletes previously exhibiting symptoms in training for
sport.123
Severe to fatal sickling cases are not limited to football
players. Sickling collapse has occurred in distance racers and
has killed or nearly killed several collegiate and high school
basketball players (including 2 women) in training, typically
during “suicide sprints” on the court, laps on a track, or a long
training run.123
The harder and faster athletes with SCT work, the earlier
and greater the sickling. Sickling can begin after only 2 to 3
minutes of sprinting—or any all-out exertion—and can quickly
increase to grave levels if the athlete struggles on or is urged on
by the coach.124
Athletes react in different ways. Some stoic athletes simply
stop and say, “I can’t go on.” When the athlete rests, sickle red
cells regain oxygen in the lungs; most sickle cells then revert to
normal shape, and the athlete soon feels good again and ready
to continue. This self-limiting feature surely saves lives.
Treatment. Complaints or evidence of exertional sickling
signs and symptoms in a working athlete with SCT should be
assumed to represent the onset of sickling and first managed by
cessation of activity. A sickling collapse is treated as a medical
emergency. Immediate action can save lives123:
1. Check vital signs.
2. Administer high-flow oxygen, 15 L/min (if available),
with a nonrebreather face mask.
3. Cool the athlete if necessary.
4. If the athlete is obtunded or if vital signs decline, call
911, attach an AED, and quickly transport the athlete to
the hospital.125,129 Appropriate medical personnel should
start an IV.
Journal of Athletic Training
13
would bring more awareness to coaches and players
about the effects of head-down contact. Evidence Category: B
Background and Literature Review
In
Pr
es
down position and at risk of serious injury. Evidence
Category: C
8. The athlete should know, understand, and appreciate the
risk of head-down contact, regardless of intent. Formal
team education sessions (conducted by the AT, team
physician, or both with the support of the coaching staff)
should be held at least twice per season. One session
should be conducted before contact begins and the other
at the midpoint of the season. Recommended topics are
mechanisms of head and neck injuries, related rules and
penalties, the incidence of catastrophic injury, the severity of and prognosis for these injuries, and the safest
contact positions. The use of videos such as Heads Up:
Reducing the Risk of Head and Neck Injuries in Football134 and Tackle Progression135 should be mandatory.
Parents of high school athletes should be given the opportunity to view these videos. Evidence Category: C
s
Figure 2. Initiating contact with the shoulder while keeping the
head up reduces the risk of head and neck injuries.
Definition and Pathophysiology. Sudden death from a
cervical spine injury is most likely to occur in football from
a fracture-dislocation above C4. Axial loading is accepted as
the primary cause of cervical spine fractures and dislocations in
football players.136,137 Axial loading occurs secondary to headdown contact, whether intentional or unintentional, when the
cervical vertebrae are aligned in a straight column. Essentially,
the head is stopped at contact, the trunk keeps moving, and the
spine is crushed between the two. When maximum vertical
compression is reached, the cervical spine fails,138 resulting in
damage to the spinal cord.
Although the football helmet has been successful in reducing
the number of catastrophic brain injuries, it is neither the cause
nor the solution for cervical spine fractures, primarily because
with head-first impact, the head, neck, and torso decelerate nonuniformly. Even after the head is stopped, the body continues to
accelerate, and no current football helmet can effectively manage the force placed on the cervical spine by the trunk.139–141 As
identified in the 1970s, contact technique remains the critical
factor in preventing axial loading.
Prevention. Initiating contact with the shoulder while keeping the head up is the safest contact position.142–148 With the head
up, the athlete can see when and how impact is about to occur
and can prepare the neck musculature accordingly. This guideline applies to all position players, including ball carriers. The
game can be played just as aggressively with this technique but
with much less risk of serious head or neck injury. Tacklers can
still deliver a big hit, and ball carriers can still break tackles.149
A top priority for prevention is player education. Athletes
have to know, understand, and appreciate the risks of headfirst contact in football.150,151 The videos Heads Up: Reducing
the Risk of Head and Neck Injuries in Football134 and Tackle
Progression135 are excellent educational tools. Parents of high
school players should also be given the opportunity to view
these videos. Coaches have a responsibility to spend adequate
time teaching and practicing correct contact techniques with all
position players. The goal should be not merely to discourage
head-down contact but to eliminate it from the game.139
Recognition. Coaches have stated that although they have
taught players to tackle correctly, the players still tended to
lower their heads just before contact.143,144 It seems that players
have learned to approach contact with their head up, but they
need to maintain this position during contact.146,149 Instinctively,
players protect their eyes and face from injury by lowering
their heads at impact.144,146,149 Therefore, coaches must allocate
enough practice time to overcome this instinct. Players who
drop their heads at the last instant are demonstrating that they
need additional practice time with correct contact techniques in
game-like situations. In addition to teaching correct contact in
the beginning of the season, coaches should reinforce the technique regularly throughout the season.144
The increase in catastrophic cervical spine injuries in the
early 1970s was attributed to coaches teaching players to initiate contact with their face masks.136,150 Players did not execute
maneuvers as they were taught, often unintentionally, and they
lowered their heads just before impact, resulting in increased
exposure to axial loading and cervical spine fractures. The
Recognition
9. Attempts to determine a player’s intent regarding intentional or unintentional head-down contact are subjective.
Therefore, coaching, officiating, and playing techniques
must focus on decreasing all head-down contact, regardless of intent. Evidence Category: C
10.Officials should enforce existing helmet contact rules
to further reduce the incidence of head-down contact. A
clear discrepancy has existed between the incidence of
head-down or head-first contact and the level of enforcement of the helmet contact penalties. Stricter officiating
14
Volume 47 • Number 1 • February 2012
LIGHTNING SAFETY
Recommendations
Prevention
Background and Literature Review
Definition. Lightning is a natural phenomenon that most
people observe within their lifetimes. One of the most dangerous natural hazards encountered, it causes more than 60 fatalities and hundreds of injuries annually in the United States.169,175
Lightning occurs with greater frequency in the southeastern United States, the Mississippi and Ohio river valleys, the
Rocky Mountains, and the Southwest,175 but no location is truly
safe from the hazard of lightning. Lightning is most prevalent
from May through September, with most fatalities and trauma
reported in July.169,175,176 Most deaths and injuries are recorded
between 10:00 am and 7:00 pm, when many people are engaged
in outdoor activities.159,169,177
Lightning can occur from cloud to cloud or cloud to ground.
Injuries and deaths are often attributed to cloud-to-ground
lightning, but compared with cloud-to-cloud lightning, it occurs
only 30% of the time. Negatively charged ionized gas builds up
in clouds and seeks objects on the earth (eg, people, houses,
trees) that have positively charged regions. When the 2 channels meet, lightning is produced, and an audible repercussion
is created; we know this as thunder.170,178 The lightning channel
has an average peak current of 20 000 A and is 5 times hotter
than the surface of the sun.170,178
Prevention. Prevention of lightning injury is simple: Avoid
the risk of trauma by staying completely indoors in a substantial building where people live and work.160,162 A proactive
lightning-specific safety policy is paramount to preventing
lightning-specific injury. The policy should identify a weather
watcher whose job is to look for deteriorating conditions. The
weather watcher must have the unchallengeable authority to
clear a venue when conditions are unsafe.161 In addition to onsite observations for deteriorating conditions, use of federal
weather monitoring Web sites is encouraged. Safe buildings
must be identified before outdoor activity begins.161,162,179 The
lightning safety plan must allow sufficient time to safely move
people to the identified building, and this time frame should
be adjusted according to the number of people being moved.
For example, moving a soccer team to safety takes less time
than moving a football team. It is also critical to remain wholly
within the safe building for at least 30 minutes after the last
sighting of lightning and sound of thunder.166,168
Treatment. People who have been struck by lightning are
safe to touch and treat and do not carry an electric charge. However, rescuers themselves are vulnerable to a lightning strike
while treating victims during active thunderstorms. Treatment
of lightning strike patients includes establishing and maintaining normal cardiorespiratory status.161,162,171,173,174 Patients may
present in asystole, pulseless, and with fixed and dilated pupils.
In
Pr
es
1. The most effective means of preventing lightning injury
is to reduce the risk of casualties by remaining indoors
during lightning activity. When thunder is heard or lightning seen, people should vacate to a previously identified safe location.159–161 Evidence Category: A
2. Establish an EAP or policy specific to lightning safety.161,162 Evidence Category: C
3. No place outdoors is completely safe from lightning, so
alternative safe structures must be identified. Sites that
are called “shelters” typically have at least one open side
and therefore do not provide sufficient protection from
lightning injury. These sites include dugouts; picnic, golf,
or rain shelters; tents; and storage sheds.160,163,164 Safe
places to be while lightning occurs are structures with
4 substantial walls, a solid roof, plumbing, and electric
wiring—structures in which people live or work.160,164
Evidence Category: B
4. Buses or cars that are fully enclosed and have windows
that are completely rolled up and metal roofs can also
be safe places during a lightning storm.165 Evidence Category: B
5. People should remain entirely inside a safe building or
vehicle until at least 30 minutes have passed since the
last lightning strike or the last sound of thunder.166,167
Evidence Category: A
6. People injured by lightning strikes while indoors were
touching electric devices or using a landline telephone or
plumbing (eg, showering). Garages with open doors and
rooms with open windows do not protect from the effects
of lightning strikes.159,161,168–170 Evidence Category: B
safe from imminent lightning strikes.171,172 Evidence Category: A
8. Triage first lightning victims who appear to be dead.
Most deaths are due to cardiac arrest.171,173,174 Although
those who sustain a cardiac arrest may not survive due to
subsequent apnea, aggressive CPR and defibrillation (if
indicated) may resuscitate these patients. Evidence Category: A
9. Apply an AED and perform CPR as warranted.174 Evidence Category: A
10.Treat for concussive injuries, fractures, dislocations, and
shock.14,164 Evidence Category: A
s
teaching of face-first contact remains a rule violation at the
high school level and is a concern at all levels of football.
Adequate enforcement of the helmet contact rules will further reduce the risk of catastrophic injuries.142–144,152–154 Both the
National Collegiate Athletic Association and the National Federation of State High School Associations have changed their
helmet contact penalties multiple times in the past 5 years155
to resolve the dilemma for officials trying to distinguish between intentional and unintentional helmet contact. The current rules for both organizations are now more complete and
concise.
A discrepancy has existed between enforcement of the helmet contact penalties and the incidence of head-down contact.
Contact with the top of the helmet has been observed in 40%
of plays146 and 18% of helmet collisions in 2007.156 In contrast,
NCAA Division I officials called 1 helmet contact penalty
in every 75 games in 2007.157 If illegal helmet contact is not
penalized, the message is that the technique is acceptable.158
Therefore, football officials must continue to improve the enforcement of these penalties.
Treatment and Management
7. Victims are safe to touch and treat, but first responders
must ensure their own safety by being certain the area is
Journal of Athletic Training
15
SUDDEN CARDIAC ARREST
Recommendations
Prevention
Recognition
In
Pr
3. Sudden cardiac arrest (SCA) should be suspected in any
athlete who has collapsed and is unresponsive. A patient’s airway, breathing, circulation, and heart rhythm
(using the AED) should be assessed. An AED should be
applied as soon as possible for rhythm analysis. Evidence
Category: B
4. Myoclonic jerking or seizure-like activity is often present after collapse from SCA and should not be mistaken
for a seizure. Occasional or agonal gasping should not be
mistaken for normal breathing. Evidence Category: B
Management
5. Cardiopulmonary resuscitation should be provided while
the AED is being retrieved, and the AED should be applied as soon as possible. Interruptions in chest compressions should be minimized by stopping only for rhythm
analysis and defibrillation. Treatment should proceed in
accordance with the updated American Heart Association
guidelines,182 which recommend that health care professionals follow a sequence of chest compressions (C), airway (A), and breathing (B). Evidence Category: B
16
Definition, Epidemiology, and Pathophysiology. Sudden
cardiac death (SCD) is the leading cause of death in exercising
young athletes.183,184 The underlying cause of SCD is usually
a structural cardiac abnormality. Hypertrophic cardiomyopathy and coronary artery anomalies are responsible for approximately 25% and 14% of SCD, respectively, in the United
States.183 Commotio cordis accounts for approximately 20% of
SCD in young athletes; caused by a blunt, nonpenetrating blow
to the chest, it induces ventricular arrhythmia in an otherwise
normal heart.183 Other structural anomalies that can cause SCD
include myocarditis, arrhythmogenic right ventricular dysplasia, Marfan syndrome, valvular heart disease, dilated cardiomyopathy, and atherosclerotic coronary artery disease. In 2% of
athletes with SCD, a postmortem examination fails to identify a
structural abnormality. These deaths may result from inherited
arrhythmia syndromes and ion channel disorders or familial
catecholaminergic polymorphic ventricular tachycardia.183
The incidence of SCD in high school athletes is estimated to
be 1:100 000 to 1:200 000.184,185 In collegiate athletes, this incidence is slightly higher, with estimates ranging from 1:65 000
to 1:69 000.184,186 A recent report185 described the incidence of
SCD in National Collegiate Athletic Association student–
athletes as 1:43 000, with higher rates in black athletes (1:1700)
and male basketball players (1:7000). Unfortunately, because
we have no mandatory national reporting system, the true incidence of SCD is unknown and probably underestimated. The
reports demonstrating the greatest incidence have estimated up
to 110 deaths each year in young athletes, equating to 1 death
every 3 days in the United States.187
Prevention. Preparticipation screening is one strategy available to prevent SCD, but the best protocol to screen athletes
is highly debated, and some methods lack accuracy. As many
as 80% of patients with SCD are asymptomatic until sudden
cardiac arrest occurs,188,189 suggesting that screening by history
and physical examination alone may have limited sensitivity
to identify athletes with at-risk conditions. Further research is
needed to understand whether additional tests such as electrocardiograms and echocardiograms improve sensitivity and can
be performed with acceptable cost-effectiveness and an acceptable false-positive rate. Detection of asymptomatic conditions
should be improved with standardized history forms and attention to episodes of exertional syncope or presyncope, chest
pain, a personal or family history of sudden cardiac arrest or
a family history of sudden death, or exercise intolerance; selective use of electrocardiograms in high-risk athletes; and a
stronger knowledge base for health care professionals.
In 2007, the American Heart Association released a helpful
12-point preparticipation cardiovascular screen for competitive
athletes based on the medical history and physical examination
(Table 3).
Emergency Preparedness. Preparation is the key to survival once SCA has occurred. Public access to AEDs and established EAPs greatly improve the likelihood of survival. All
necessary equipment should be placed in a central location that
is highly visible and accessible; multiple AEDs may be needed
for larger facilities. An EAP should be in place and specific to
each athletic venue and should include an effective communication system, training of likely first responders in CPR and
AED use, acquisition of the necessary emergency equipment,
a coordinated and practiced response plan, and access to early
es
1. Access to early defibrillation is essential. A goal of less
than 3–5 minutes from the time of collapse to delivery of
the first shock is strongly recommended. Evidence Category: B
2. The preparticipation physical examination should include the completion of a standardized history form and
attention to episodes of exertional syncope or presyncope, chest pain, a personal or family history of sudden
cardiac arrest or a family history of sudden death, and
exercise intolerance. Evidence Category: C
Background and Literature Review
s
Therefore, CPR should be continued even when defibrillation
with an AED is not indicated (eg, asystole). Advanced cardiac
life support, medications, intubation, and continued CPR may
resuscitate these victims. People with a Glasgow Coma Scale
score as low as 5 have survived after aggressive resuscitation.180
After a lightning strike, many patients present with symptoms
resembling a concussion. Some may have temporary paralysis,
hearing loss, or skin markings, yet true burns are rare. Patients
should be assessed and treated for concussion, fractures, dislocations, and shock.174
Return to Play. Lightning strike patients are eligible to return to previous activities upon release by a qualified physician.
Many never seek treatment and do not need hospitalization. If
orthopaedic injuries are present, recovery follows the typical
protocols. More often than not, however, patients experience
neurologic sequelae and have difficulty returning to their preinjury levels.175,181 They may never fully return to desired levels,
and they need consistent and perhaps multidisciplinary medical
and psychological follow-up.174,181
Volume 47 • Number 1 • February 2012
Medical historya
Personal history
1. Exertional chest pain/discomfort
2. Unexplained syncope/near-syncopeb
3. Excessive exertional and unexplained dyspnea/fatigue,
associated with exercise
4. Prior recognition of a heart murmur
5. Elevated systemic blood pressure
Family history
6. Premature death (sudden and unexpected, or otherwise) before
age 50 years due to heart disease, in ≥1 relative
7. Disability from heart disease in a close relative <50 years of age
8. Specific knowledge of certain cardiac conditions in family
members: hypertrophic or dilated cardiomyopathy, long-QT
syndrome or other ion channelopathies, Marfan syndrome, or
clinically important arrhythmias
Physical examination
9. Heart murmurc
10. Femoral pulses to exclude aortic coarctation
11. Physical stigmata of Marfan syndrome
12. Brachial artery blood pressure (sitting position)d
ACKNOWLEDGMENTS
We gratefully acknowledge the efforts of Gianluca Del Rossi,
PhD, ATC; Jonathan Drezner, MD; John MacKnight, MD; Jason
Mihalik, PhD, ATC; Francis O’Connor, MD, MPH; and the Pronouncements Committee in the preparation of this document.
es
a
Parental verification is recommended for high school and middle
school athletes.
b
Judged not to be neurocardiogenic (vasovagal); of particular concern when related to exertion.
c
Auscultation should be performed in both supine and standing
positions (or with Valsalva maneuver), specifically to identify murmurs
of dynamic left ventricular outflow tract obstruction.
d
Preferably taken in both arms (Kaplan NM, Gidding SS, Pickering
TG, Wright JT Jr. Task Force 5: systemic hypertension. J Am Coll Cardiol. 2005;45(8):1346–1348).
Reprinted with permission from Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive
athletes: 2007 update. Circulation. 2007;115(12):1643–1655.
respiration or occasional gasping should not be mistaken for
normal breathing and should be recognized as a sign of SCA193;
myoclonic jerking or seizure-like activity shortly after collapse
should also be treated as SCA until proven otherwise.194,195 If
no pulse is palpable, the patient should be treated for SCA, and
CPR should be initiated.
Treatment. In any athlete who has collapsed and is unresponsive, SCA should be suspected. If normal breathing and
pulse are absent, CPR should be started immediately and EMS
activated. The CPR should be performed in the order of CAB
(chest compressions, airway, breathing) by medical professionals (hands-only CPR is now recommended for lay responders) while waiting for arrival of the AED and stopped only for
rhythm analysis and defibrillation. This should continue until
either advanced life support providers take over or the victim
starts to move.193,194,196,197 Early detection, prompt CPR, rapid
activation of EMS, and early defibrillation are vital to the athlete’s survival. For any athlete who has collapsed and is unresponsive, an AED should be applied as soon as possible for
rhythm analysis and defibrillation if indicated. The greatest
factor affecting survival after SCA arrest is the time from arrest to defibrillation.195,196 Survival rates have been reported at
41%–74% if bystander CPR is provided and defibrillation occurs within 3 to 5 minutes of collapse.186,194,196–207
Certain weather situations warrant special consideration. In
a rainy or icy environment, AEDs are safe and do not pose a
shock hazard. However, a patient lying on a wet surface or in a
puddle should be moved. A patient lying on a metal conducting
surface (eg, stadium bleacher) should be moved to a nonmetal
surface. If lightning is ongoing, rescuers must ensure their
safety by moving the patient indoors if possible.
s
Table 3. The 12-Element AHA Recommendations for
Preparticipation Cardiovascular Screening of Competitive
Athletes
In
Pr
defibrillation. It should identify the person or group responsible
for documentation of personnel training, equipment maintenance, actions taken during the emergency, and evaluation of
the emergency response.192 The EAP should be coordinated
with the local EMS agency and integrated into the local EMS
system. It should also be posted at every venue and near appropriate telephones and include the address of the venue and
specific directions to guide EMS personnel.
Assessment. Differential diagnosis of nontraumatic exerciserelated syncope or presyncope includes sudden cardiac arrest,
EHS, heat exhaustion, hyponatremia, hypoglycemia, exerciseassociated collapse, exertional sickling, neurocardiogenic
syncope, seizures, pulmonary embolus, cardiac arrhythmias,
valvular disorders, coronary artery disease, cardiomyopathies,
ion channel disorders, and other structural cardiac diseases.
In any athlete who has collapsed in the absence of trauma,
suspicion for sudden cardiac arrest should be high until normal airway, breathing, and circulation are confirmed. Agonal
DISCLAIMER
The NATA publishes its position statements as a service to
promote the awareness of certain issues to its members. The information contained in the position statement is neither exhaustive nor exclusive to all circumstances or individuals. Variables
such as institutional human resource guidelines, state or federal
statutes, rules, or regulations, as well as regional environmental conditions, may impact the relevance and implementation
of these recommendations. The NATA advises its members
and others to carefully and independently consider each of the
recommendations (including the applicability of same to any
particular circumstance or individual). The position statement
should not be relied upon as an independent basis for care but
rather as a resource available to NATA members or others.
Moreover, no opinion is expressed herein regarding the quality
of care that adheres to or differs from NATA’s position statements. The NATA reserves the right to rescind or modify its
position statements at any time.
Journal of Athletic Training
17
Appendix. National Athletic Trainers’ Association Statements a
Citation
Safe weight loss and
maintenance practices in
sport and exercise (2011)
Sammarone Turocy P, DePalma BF, Horswill CA, et
al. National Athletic Trainers’ Association position
statement: safe weight loss and maintenance
practices in sport and exercise. J Athl Train.
2011;46(3):322–336.
Valovich McLeod TC, Decoster LC, Loud KJ, et al.
National Athletic Trainers’ Association position
statement: prevention of pediatric overuse injuries.
J Athl Train. 2011;46(2):206–220.
Zinder SM, Basler RSW, Foley J, Scarlata C, Vasily
DB. National Athletic Trainers’ Association
position statement: skin diseases. J Athl Train.
2010;45(4):411–428.
Swartz EE, Boden BP, Courson RW, et al. National
Athletic Trainers’ Association position statement:
acute management of the cervical spine–injured
athlete. J Athl Train. 2009;44(3):306–331.
Bonci CM, Bonci LJ, Granger LR, et al. National Athletic
Trainers’ Association position statement: preventing,
detecting, and managing disordered eating in
athletes. J Athl Train. 2008;43(1):80–108.
Cappaert TA, Stone JA, Castellani JW, Krause BA,
Smith D, Stephens BA. National Athletic Trainers’
Association position statement: environmental
cold injuries. J Athl Train. 2008;43(6):640–658.
Anderson S, Eichner ER. Consensus statement: sickle
cell trait and the athlete.b
Drezner JA, Courson RW, Roberts WO, Mosesso VN,
Link MS, Maron BJ. Inter-Association Task Force
Recommendations on emergency preparedness
and management of sudden cardiac arrest in high
school and college athletic programs: a consensus
statement. J Athl Train. 2007;42(1):143–158.
Jimenez CC, Corcoran MH, Crawley JT, et al. National
Athletic Trainers’ Association position statement:
management of the athlete with type I diabetes
mellitus. J Athl Train. 2007;42(4):536–545.
Miller MG, Weiler JM, Baker R, Collins J, D’Alonzo
G. National Athletic Trainers’ Association position
statement: management of asthma in athletes.
J Athl Train. 2005;40(3):224–245.
Heck JF, Clarke KS, Peterson TR, Torg JS, Weis MP.
National Athletic Trainers’ Association position
statement: head-down contact and spearing in
tackle football. J Athl Train. 2004;39(1):101–111.
Guskiewicz KM, Bruce SL, Cantu RC, et al. National
Athletic Trainers’ Association position statement:
management of sport-related concussion. J Athl
Train. 2004;39(3):280–297.
Andersen JC, Courson RW, Kleiner DM, McLoda TA.
National Athletic Trainers’ Association position
statement: emergency planning in athletics. J Athl
Train. 2002;371(1):99–104.
Binkley HM, Beckett J, Casa DJ, Kleiner DM, Plummer
PE. National Athletic Trainers’ Association position
statement: exertional heat illnesses. J Athl Train.
2002;37(3):329–342.
Casa DJ, Armstrong LE, Hillman SK, et al. National
Athletic Trainers’ Association position statement:
fluid replacement for athletes. J Athl Train. 2000;
35(2):212–224.
Walsh KM, Bennett B, Cooper MA, Holle RL, Kithil R,
Lopez RE. National Athletic Trainers’ Association
position statement: lightning safety for athletics
and recreation. J Athl Train. 2000;35(4):471–477.
Preventing, detecting, and
managing disordered
eating in athletes (2008)
Environmental cold injuries
(2008)
Sickle cell trait and the
athlete (2007)
Emergency preparedness
and management of
sudden cardiac arrest in
high school and college
athletic programs (2007)
Management of the athlete
with type I diabetes
mellitus (2007)
Management of asthma in
athletes (2005)
Head-down contact and
spearing in tackle
football (2004)
Management of sportrelated concussion
(2004)
Emergency planning in
athletics (2002)
Exertional heat illness (2002)
Fluid replacement for
athletes (2000)
Lightning safety for athletics
and recreation (2000)
a
b
es
Acute management of the
cervical spine–injured
athlete (2009)
Pr
Skin diseases (2010)
In
Prevention of pediatric
overuse injuries (2011)
URL
s
Topic (Year)
http://www.nata.org/sites/default/files/JAT-46-3-16
-turocy-322-336.pdf
http://www.nata.org/sites/default/files/Pediatric
-Overuse-Injuries.pdf
http://www.nata.org/sites/default/files/position
-statement-skin-disease.pdf
http://www.nata.org/sites/default/files/acutemgmt
ofcervicalspineinjuredathlete.pdf
http://www.nata.org/sites/default/files/Preventing
DetectingAndManagingDisorderedEating.pdf
http://www.nata.org/sites/default/files/Environmental
ColdInjuries.pdf
http://www.nata.org/sites/default/files?SickleCell
TraitAndTheAthlete.pdf
http://www.nata.org/sites/default/files/sudden
-cardiac-arrest-consensus-statement.pdf
http://www.nata.org/sites/default/files/MgmtOf
AthleteWithType1DiabetesMellitus.pdf
http://www.nata.org/sites/default/files/MgmtOf
AsthmaInAthletes.pdf
http://www.nata.org/sites/default/files/Head
DownContactAndSpearingInTackleFB.pdf
http://www.nata.org/sites/default/files?MgmtOfSport
RelatedConcussion.pdf
http://www.nata.org/sites/default/files/Emergency
PlanningInAthletics.pdf
http://www.nata.org/sites/default/files/External
HeatIllnesses.pdf
http://www.nata.org/sites/default/files/Fluid
ReplacementsForAthletes.pdf
http://www.nata.org/sites/default/files/Lightning
Safety4AthleticsRec.pdf
Updated position statements are posted at www.nata.org. Readers should check the Web site for the most current versions.
Available online only.
18
Volume 47 • Number 1 • February 2012
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